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The behavior of the weight of the heart and the blood pressure of albino rats under different conditions

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... The increase in body weight in the control group produced an expected increase in left ventricular weight and a decrease in LV/BW ratio. The LV/BW ratio naturally decreases with an increase in body weight [39,40]. Since animals in this study were age-matched, differences in their LV/BW ratio reflect differences in body weight and not significant changes in the circulation [39,40]. ...
... The LV/BW ratio naturally decreases with an increase in body weight [39,40]. Since animals in this study were age-matched, differences in their LV/BW ratio reflect differences in body weight and not significant changes in the circulation [39,40]. ...
Article
Introduction. Increased adiposity is an important risk factor for erectile dysfunction (ED) and cardiovascular disease (CVD). Although accumulation of visceral adipose tissue (VAT) is recognized as a key mediator in the pathogenesis of CVD, its role in ED has not been elucidated. Aim. To determine whether caloric restriction (CR) could prevent VAT accumulation and thereby prevent the onset of ED in normotensive rats. Methods. Male Sprague Dawley rats (10 weeks) were randomized into three dietary groups: ad libitum control (CON), mild CR (CRMI), and moderate CR (CRMOD). Body weight (BW), body length abdominal girth (AG), and VAT (g-magnetic resonance imaging based) were assessed longitudinally. Erections were assessed using the apomorphine bioassay (80 µg/kg, SQ) after 20 weeks of CR. Excised VAT (mesenteric, epididymal, omental, and retroperitoneal), the internal pudendal artery (IPA) and serum were collected postmortem. Structure and function of the IPA was assessed at study end. Main Outcome Measures. Erectile responses, adiposity (VAT), abdominal girth, serum analysis. Results. BW (CON = 653 ± 58.6 g; CRMI = 535 ± 47.4 g; CRMOD = 409 ± 17.4 g) and VAT (CON = 39 ± 9.0 g; CRMI = 30 ± 9.9 g; CRMOD = 14 ± 3.5 g) were markedly different between the three groups. AG significantly correlated with longitudinal changes in VAT (R2 = 0.61) and excised VAT (R2 = 0.87). CR preserved erectile responses (CON = 0.6 ± 0.45, CRMI = 1.2 ± 0.77 g, CRMOD = 2.5 ± 0.43 g). A strong inverse correlation between VAT (%) and erectile function was found (R2 = 0.74) whereas BW was less predictive of ED (R2 = 0.48). There were no changes in traditional biomarkers (glucose, lipids) which could account for the ED. IPA structure was not different between groups, while CRMOD preserved endothelial function. Conclusions. CR effectively prevented VAT accumulation in normotensive rats. Independently of changes in other metabolic markers, this intervention ameliorated the negative impact on erectile responses that occurs with age. Functional changes of the IPA may be a key mechanism by which erections are preserved with CR. AG was shown to be a strong index of VAT in rats. Maio MT, Hannan JL, Komolova M, and Adams MA. Caloric restriction prevents visceral adipose tissue accumulation and maintains erectile function in aging rats. J Sex Med 2012;9:2273–2283.
... Clinical, experimental, and therapeutic efforts regarding LVH have typically centered on mechanisms involved with its development. Traditional approaches suggest that LVH results from biomechanical stress of the heart [5, 6]. If this stress is removed, regression of LVH is possible. ...
Article
Although a host of studies catalogue changes that occur with the development of left ventricular hypertrophy (LVH), there is little information about features related solely to LVH regression. This is due, in part, to a lack of animal models to study this question. While traditional models of aortic banding have provided useful information regarding the development of LVH, a similarly effective model is necessary to study mechanisms associated with LVH regression. Minimally invasive transverse arch banding was performed in C57BL6 mice using a slipknot technique. Twenty-eight days later, the band was removed. Carotid Doppler velocity gradients were serially measured to assess the degree of aortic constriction. Echocardiography, histology, electron microscopy, and real-time polymerase chain reaction were used to assess functional, structural, and genetic aspects of hypertrophy. Banding of the transverse arch created the expected increase in aortic velocity and gradient between the left and right carotid artery, which normalized with relief of the constriction. Pressure overload resulted in a robust hypertrophic response as assessed by heart weight/body weight ratios, gross and microscopic histology, transthoracic echocardiography, electron microscopy, and hypertrophy gene expression. These markers were reversed within 1 week following debanding and were maintained for up to 4 weeks. Mortality rate for the cumulative procedure was 5% over a 2-month period. These results demonstrate a safe, effective, and reproducible method of promoting LVH regression-avoiding the need for endotracheal intubation, mechanical ventilation, and a second invasive surgery to remove the constriction. The simplicity of this technique combined with the well-known advantages of using the mouse species makes this model both unique and relevant. Ultimately, this model will facilitate focused study of independent mechanisms involved with LVH regression.
... Beznak (1955) reported that aortic constriction in rats produced a thirty-two percent increase in heart weight in five days. In addition, both Rather (1949) and Beznak (1954) found that the relationship between body weight and heart weight in rats was maintained regardless of whether the animals gained or lost weight (starvation). Thus it would appear that any cardiac stress due to the ligations in the hens should have resulted in some discernible cardiac hypertrophy after two weeks. ...
Article
Full-text available
OCCLUSION of both the carotid and vertebral arteries has been shown not to be fatal in all animals tested. This, of course, indicates that collateral circulation is capable of supplying the head with sufficient blood to sustain life. Taylor and Page (1951) ligated both common carotid and vertebral arteries in eleven dogs. Ten of the dogs lived; however, they appeared dazed, listless and often not interested in food or drink for several days after ligation. Bunce (1960) ligated and then sectioned the carotid and vertebral arteries in fourteen dogs as follows: seven dogs, both common carotids and vertebrals; two dogs, both common carotids; two dogs, both vertebrals; two dogs, both internal carotids and vertebrals; one dog, both common carotids and one vertebral. All of the dogs lived for at least four months, but the seven animals with both common carotids and vertebrals sectioned showed impaired intelligence and alertness, poor physical . . .
... The cortisol was much more effective than the mineralocorticoid Percorten. On the other hand, adrenalectomized rats do not develop arterial hypertension after constriction of the aorta abdominalis (Beznfik, 1954). Therefore, it seems to be possible, but not certain, that adrenocortical hormones modify the metabolic processes of the heart in the early stage of hypertrophy (Fizel and Fizelova, 1972). ...
Article
Male Wistar rats were treated with high cortisol doses for 1 week. The dose administered daily was 15 mg per animal in group 1 (7 animals) and 30 mg in group 2 (7 animals). 7 rats served as control group. After cortisol treatment the body weights decreased due to skeletal muscle catabolism and the heart weights increased. Morphometric analysis of the left ventricular posterior papillary muscles gave evidence that the increased heart weights resulted from an increased number of mitochondria and an increased volume of the cytoplasm, whereas the myofibrillar mass was not affected. The surface area of inner mitochondrial membranes (+cristae mitochondriales) per myofibrillar unit volume increased from 15.7 2/3 to 21.3 2/3 in group 1 and 21.4 2/3 in group 2. Ultrastructural changes indicating myocardial cell damage were absent. Similar quantitative results have been reported to occur in the early phase of cardiac overload. For elucidating the hemodynamic effects of glucocorticoid a second experiment was performed: 7 Wistar rats were treated with cortisol in the same way as group 1, 7 others of the same body weight served as control. The systolic arterial pressure was significantly elevated in the cortisol group. Though myocardial tissue is known to be able to accumulate large quantities of glucocorticoids our results indicate that the application of high cortisol doses for a short time does not produce myocardial cell damage and does not suppress the myocardial adaption to the glucocorticoid-induced hypertension, i.e. hypertrophy. On the contrary, it seems to be possible that the adaption process is itself facilitated or accelerated by the presence of high cortisol concentrations in the heart. This thesis is supported by the considerably higher relative heart weights in the cortisol groups and is in agreement with observations reported by other authors.
Article
Previous studies have reported that potassium depletion arrests both body and heart growth, and that aortic ligation can induce myocardial potassium loss. To examine the effects of potassium depletion on the cardiac growth response to an increase in pressure load, we induced severe potassium depletion in rats by dietary means for 3 weeks and then subjected them to aortic ligation. 3 weeks following ligation and after a total of 6 weeks of continued potassium deprivation, the animals were sacrificed. Our results show that after aortic ligation the left ventricular weight in potassium depleted rats significantly increased by an average of 155 mg, a value which was somewhat less than the 208-mg increase observed in normokalemic animals. The presence of focal myocardial necrosis in hypokalemic rats, accordingly, did not appear to prevent the increase in ventricular mass induced by augmented pressure load. Furthermore, despite marked reduction in skeletal muscle potassium content there was no decrease in the myocardial potassium content even after aortic ligation. We conclude that profound dietary potassium depletion for a prolonged period of 6 weeks does not impede the cardiac growth response to an increase in pressure load.
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A new technique for producing progressive stenosis of the aorta in rabbits is described. The results indicate a marked hypertrophy is evident 20 to 30 days after surgery with the eventual development of congestive failure.
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Scalar electrocardiograms and vectorcardiograms were performed on children with isolated congenital heart defects just before corrective surgery, 7 to 10 days after surgery, and 6 to 18 months later. The early and late changes were statistically analyzed. In 36 cases of pulmonary stenosis there was a reduction of right ventricular hypertrophy in early and late cardiograms. In 42 cases of secundum atrial defect no significant reduction of right ventricular hypertrophy was shown in the early cardiograms, although the late cardiograms did show this effect; voltages from the left ventricle were significantly increased in both the early and late cardiograms. In 49 cases of patent ductus arterious left ventricular hypertrophy was reduced in the early and late cardiograms. In 39 cases of valvular aortic stenosis a reduction of the S in V1 was seen in the early ECG and there was a significant reduction of left ventricular hypertrophy in the late cardiograms. The very rapid reduction of hypertrophy was surprising and may be explained by electrical phenomena or atrophy of the ventricle.
Article
The roles of selected hormones in restoring the capacity of the remaining kidney following uninephrectomy of hypophysectomized rats to respond by tubular hyperplasia were explored. Autoradiography, using tritiated thymidine, was employed for identifying cells synthesizing new deoxyribonucleic acid within a standard period, a valid measure of mitotic activity. For animals with intact pituitary glands, both cortex and medulla of kidneys remaining three days after uninephrectomy exhibited a 3½-fold increase in numbers of labeled cells over control levels. The amount of mitotic activity in either region of bilaterally intact kidneys of hypophysectomized animals was not significantly different from that for animals with intact pituitaries, but the compensatory renal hyperplastic response to uninephrectomy was reduced to one-third. Either a small amount of growth hormone or a much larger amount of anterior pituitary extract, administered subcutaneously twice daily for several days, restored the compensatory response to uninephrectomy to levels obtained in rats with intact hypophyses. Adrenocorticotropic hormone depressed mitosis markedly in control kidneys of hypophysectomized animals and to an even lower level in remaining kidneys. Growth hormone would appear to be a necessary and effective component of the pituitary secretion in permitting compensatory renal hyperplasia to take place. Since prior studies have shown adrenalectomy to promote cellular division in renal tubules, it was assumed that the presently reported depression of renal mitosis by excess adrenocorticotropic hormone was mediated by an overactivity of the adrenal glands.
Article
Studies were conducted with hypophysectomized rats to determine the effects of chronic exercise (training), injections of exogenous hormones, aortic constrictions and combinations there of on the weight of the heart. In addition, the role of growth hormone on cardiac weight was reinvestigated. The hypophysectomized rats that were trained for 10 weeks or longer had significantly heavier heart weights than their nontrained counterparts. When daily injections of a single exogenous hormone of ACTH, GH, ICSH or TSH were made into trained and nontrained animals, there was no trained group that had significantly heavier heart weights than their control group. Rats having aortic constrictions or receiving DOCA injections also had significantly heavier heart weights than their controls. When various dosages of GH (0.2 mg to 6.0 mg) were injected daily for three weeks, no evidence was obtained that indicated that the presence of this hormone resulted in cardiac enlargement. It was concluded that under the experimental condition of this study, cardiac enlargement can occur in hypophysectomized rats when the work demands on the heart have been increased.
Article
The effect of anorexia on the weights and water levels of body organs was determined. Ninety-two adult female albino rats of a Wistar strain were divided into groups which were subjected to various daily restrictions of food intake that resulted in a loss of body weight up to 40% at the end of 2 weeks when they were killed and autopsied. At autopsy the wet weight and water content of the following organs were measured: adrenal glands, brain, cardiac stomach, pyloric stomach, small bowel, cecum, colon, heart, kidneys, liver, lungs, muscle, ovaries, skin, spleen, salivary glands, thymus gland and residual carcass. Up to 20% loss of body weight, the effects of starvation were of a minor nature. At 30 to 40%, gastric ulcers and a stress reaction appeared, and most organs had lost considerable dry weight and gained water; but only brain showed no changes in weight.
Article
The normal heart has the capacity to either augment or reduce its mass in relation to long-term alterations in hemodynamic and metabolic demands. However, once cardiac hypertrophy is established, as in hypertensive heart disease, it is less clear whether the augmented mass can revert to normal with control of arterial pressure. In experimental models in which systemic hypertension is induced in genetically normotensive animals, left ventricular weight generally returns toward normal with the removal of the inciting stimulus for the hypertension. However, when arterial pressure control is achieved by pharmacologic therapy, and the inciting stimulus (mechanical or genetic) is intact, the results of pressure reduction on ventricular weight are much more variable than that observed with the removal of a mechanical stimulus for hypertension. It is hypothesized that pharmacologic pressure reduction elicits secondary adjustments in cardiorenal and neurohumoral function which have important influences on ventricular hypertrophy.
Article
Cardiomegaly was observed in rats severely intoxicated with ethanol for a 4 day period. It was apparent at 48 hours of treatment, a time at which cardiac protein was elevated and continued into withdrawal. During a 4 day abstinence period the degree of hypertrophy declined towards normal. Cardiac noradrenaline was reduced at the 48 hour time of intoxication, then increased gradually in the further experimental period. As the cardiac hypertrophy occurs at a time that urinary catecholamines are elevated and the adrenal medulla is intensely stimulated, it is proposed that increased levels of circulating catecholamines are largely responsible for the enlargement of the heart.
Article
Male guinea pigs were exposed continuously to 5°C for 2–18 weeks (BW=239–1074 g) or to an ambientPO2=80 mm Hg for 2–14 weeks (BW=244–965g). Control guinea pigs were kept at 22°C and an average ambientPO2 of 133 mm Hg. The right and the left ventricular free walls were separated from the septum and weighed (RVW and LVW). Myoglobin concentrations [Mb] of the right and the left ventricles were measured. In all animals, total heart weights (THW), RVW and LVW were linearly related to BW. In the control animals, ventricular [Mb] increased with BW for 2–3 weeks after birth but remained unchanged thereafter. In the 5°C animals, after 4 weeks of exposure, [Mb] in the right and the left ventricles was significantly higher than that of the controls. THW also was significantly higher in the 5°C animals. Furthermore, this cold-induced cardiac hypertrophy was due to both right and left ventricular hypertrophy. In hypoxia-acclimated animals, after 14 weeks of exposure toPO2=80 mm Hg, the [Mb] of the RV was significantly higher than that of the controls, whereas there was no significant difference between the [Mb] of the LV of the control and hypoxic animals. THW was significantly higher in the hypoxic guinea pigs than in the controls or the 5°C animals. The hypoxia-induced cardiac hypertrophy was due to a marked right ventricular hypertrophy while LVW was significantly lower in the hypoxic animals than in the controls
Article
A heart-lung preparation with flow limited to the coronary vessels was used to study cardiac performance 4 to 120 days after severe constriction of the abdominal aorta in rabbits. Cardiac performance was evaluated by finding the maximum mean arterial pressure against which the heart could pump. Cardiac performance began to exceed the normal, range by the second or third post operative week and was well above normal after the first month. A high cardiac performance was not necessarily associated with marked ventricular hypertrophy. Animals died of heart failure within the first month, and all had developed a much more rapid rate of blood pressure increase than those that survived without signs of decompensation. We conclude that the basic cause of heart failure after severe aorta constriction is a rapid rise in arterial pressure which exceeds the rate at which the heart develops an improved performance.
Article
Oxygen consumption, weight and rate of the heart, blood pressure, cardiac output and work are restored to normal if rats hypophysectomized two to three months previously are treated with thyroxine over a period of three to five weeks. Although under basal conditions the above parameters in these rats are the same as those in normal rats, the maximum output and work during loading by infusion of polyvinylpyrrolidone into the right side of the heart are less in hypophysectomized rats treated with thyroxine than they are in normal rats. Similarly, if a load is imposed on the heart by constriction of the aorta, cardiac output and work are well below the values measured in normal rats with aortic constriction. It is concluded that thyroxine treatment of hypophysectomized rats can restore to normal the performance of the cardiovascular system under basal conditions but that during loading (polyvinylpyrrolidone infusion, aortic constriction) the performance of the cardiovascular system is less than in normal rats.
Article
An acute myocarditis was produced in 48 C3H mice by infection with Trypanosoma cruzi (Colombian). Spontaneous activity was measured in activity drums, and the effects of forced muscular exercise, in the form of swimming, were studied. Fifty days after inoculation, the infected as well as the 44 control animals were sacrificed.Spontaneous activity decreased as parasitemia increased, and increased again as parasitemia subsided.The ratio of heart weight to body weight was increased significantly by swimming alone, and also by infection alone. The combination of both factors resulted in a significantly greater increase in the heart weight/body weight ratio than did either alone. The ratio of dry heart weight to wet heart weight was not affected by either factor.Swimming was associated with a greater mortality, with more severe and more diffuse cellular infiltration, and with a greater number of parasites in the myocardium.
Article
The effect of the cardiac distension on the heart rate was studied in two kinds of cardiac enlargement (trained rats and nutritional anemic animals) and compared with normal ones. In the trained animals the cardiac distension produced an increase in the cardiac rate while no modifications were observed in the nutritional anemic rats. These results are different to those obtained in the renal hypertensive rats where the cardiac distention produced bradycardia. The enlargement of the hearts of the trained animals was due to an hypertrophy of the muscle fibres and in the nutritional anemic rats to an increase in the number of cells. This was established by the determination of the nucleic acids. No modifications were observed in the water and sodium contents in any of the groups studied. These results suggest that the alteration observed in the cardiac pressoreceptor reflex in hypertensive rats is not due to the enlarge-ment of the heart.
Article
The Sapirstein method was used to study the circulatory conditions of hypophysectomized rats treated with oestrogen and with vasopressin. It was found that in rats hypophysectomized for several weeks there are decreases in the blood pressure, cardiac output, renal fraction of the cardiac output and the renal blood flow. 1 hr after vasopressin injection following a 10-day oestrone pretreatment, the renal fraction of the cardiac output and the renal blood flow decreases significantly compared to the hypophysectomized untreated group, and the renal vascular resistance increases to a considerable extent. The vasoconstriction can also be detected in the kidneys of oestrone-pretreated hypophysectomized animals, following the administration of vasopressin. The protective effect of hypophysectomy against renal cortical necrosis induced by hormone treatment is therefore not exerted by means of the inhibition of the renal vasospasm. It may be presumed that after the hypophysectomy the O2 demand of the kidneys decreases and so the kidneys better endure the O2 deficiency caused by the renal vasospasm.
Chapter
Dieser Abschnitt befaßt sich nur mit den Auswirkungen, welche Störungen der Hypophysenfunktion auf das cardiovasculäre System haben können. Auf die erhebliche Bedeutung, die ihrerseits den Kreislaufstörungen für das Zustandekommen insbesondere der postpartualen Hypophysenvorderlappeninsuffizienz zukommen kann (SHEEHAN 1937, 1939, 1955 u. a.), wird im folgenden nicht eingegangen.
Chapter
Die Nahrung hat im Organismus sowohl energetische als auch spezifisch-stoffliche Aufgaben zu erfüllen. Zur Aufrechterhaltung der Lebensvorgänge ist ein ständiger Stoff- und Energieumsatz nötig. Baustoffe, energiereiche Verbindungen und Sauerstoff müssen aus der Umgebung in den Organismus aufgenommen werden. Jede energetische und substantielle Fehlbilanz in Stoffangebot oder Stoffbedarf zwingt den Organismus zum Verbrauch seiner energetischen Reserven und darüber hinaus zum Abbau von Organsubstanz, um die für die Aufrechterhaltung der Lebensprozesse notwendige Energie zu produzieren und die Abnutzungsquote zu decken.
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Die Aufgabe der morphologisch ausgerichteten Herzpathologie besteht darin, die anatomischen Substrate der Herzinsuffizienz aufzuzeigen. Bei groben herdförmigen oder diffusen Zerstörungen des Herzmuskels, z. B. bei Infarkten infolge thrombosierender Coronarsklerose oder bei schwerer Myokarditis, kann man die Funktionsstörungen des Herzens aus den morphologischen Befunden heraus gut verstehen. Aber in der Mehrzahl der Fälle von chronischer Insuffizienz, die mit Hypertrophie und Dilatation des Herzens einhergehen, sind die morphologischen Veränderungen am Myokard so geringgradig, daß ihre funktionelle Wertigkeit im Hinblick auf das Herzversagen fragwürdig erscheint.
Article
Two hundred male Sprague-Dawley rats were divided into four groups of 50 animals each. Group A served as controls; group B received 0.1 mg. of digitoxin/100 gm. body weight daily for six days of each week; group C underwent subdiaphragmatic suprarenal aortic constriction but did not receive digitoxin; and group D received doses of digitoxin similar to those given to group B, beginning five to seven days prior to aortic constriction. After suitable corrections for differences in body weight among the different groups, it became clear that digitoxin alone had no effect on the ventricular weight of the rats in group B. Although the rats in both groups C and D had ventricular weights significantly greater than control, the administration of digitoxin resulted in the development of significantly lesser degrees of myocardial hypertrophy and decreased the incidence of fatal congestive heart failure. While the development of hypertrophy represents a fundamental adaptive mechanism to a chronic pressure load placed on the ventricle, the usefulness of this adaptive mechanism may well be limited. By reducing the development of myocardial hypertrophy, digitoxin permits the ventricle to sustain an excessive hemodynamic burden with less encroachment on this fundamental reserve mechanism, thus favorably influencing cardiac function.
Article
Rats were housed in activity cages and fed 1 h daily. When these rats died, wet and dry weights were obtained for adrenals, spleen, liver, kidney, heart, stomach rumen, and stomach body. Most activity rats, as compared to food-yoke control and home-cage control rats, had lesions in the glandular stomach. Adrenal and heart weights suggested that activity rats had been subjected to some degree of stress. Characteristic starvation effects, such as rumenal lesions and edema of stomach tissue, were not observed in activity rats.
1. Animals fed a high energy ration had bigger body weight, and bigger heart, brain and genitals then animals fed a normal diet, but they had substantially smaller liver, kidneys, adrenals and thyroid glands than the otherwise smaller animals. Restricted feeding did not necessarily produce smaller organ sizes than normal. 2. The yearly variation in organ sizes was astonishingly large whereas the sex differences were rather rare. 3. For organs like liver, kidneys and thyroid glands the conclusion from the results was independent of the method of expressing the organ mass. The organ sizes seemed to be influenced by many coexisting factors like yearly differences, sex and age of animals, feed and farm.
Article
The development of cardiac hypertrophy was examined in rats that had undergone sympathectomy with 6-hydroxydopamine. After 4 days, the rats were given severely intoxicating doses of ethanol or isocalorically paired quantities of maltose-dextrin by intubation at 8-h intervals up to 48 h. The ethanol and sugar intubations were applied in a nutritionally adequate, liquid diet mix. The extent of the peripheral sympathectomy was evident from the absence of detectable quantities of noradrenaline in hearts of animals injected with the neurotoxin and in the reduced levels of excreted noradrenaline. The adrenal medullary catecholamine contents of sympathectomized rats were unchanged in the absence of ethanol; there were reduced quantities of adrenaline in the medullae of rats given ethanol. The adrenal glands of rats given ethanol were larger than those from control animals. Urine samples from sympathectomized and control rats, given ethanol, displayed equivalent increases in excreted adrenaline and noradrenaline. Increases in relative cardiac weight were evident in hearts from sympathectomized animals after 4 days of sympathectomy, and this change reached significance in the hearts from 6-hydroxydopamine-treated rats after a further 2 days on the control diet. Hearts from animals exposed to ethanol showed a marked, rapid development of cardiomegaly; after 24 h there was an increased mass of some 17%, which was sustained over the remaining 24-h period. The proportion of cardiac protein did not differ in the large hearts from ethanol-treated animals and those from their controls, hence myocardial oedema could not account for the increase in weight.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
Myocardial cellular and subcellular adaptations associated with chronic hypoxia were determined in 16 week old male normotensive Wistar-Kyoto, spontaneously hypertensive and aortic constricted rats. The animals were exposed to six weeks of hypobaric hypoxia at a simulated altitude of 6,100 (m), and their glutaraldehyde perfuse-fixed hearts compared to normoxic controls.Exposure to hypoxia abolished the hypertension associated with the spontaneously hypertensive and aortic constricted groups and reduced the mean heart rate in all three hypoxic groups. The magnitude of hypertrophy was significant and comparable in all three groups, based on heart weight and left ventricular fiber diameter measurements. While capillary density was significantly reduced in the spontaneously hypertensive and aortic constricted rats, exposure to hypoxia facilitated an absolute increase in the number of capillaries of the hypoxic spontaneously hypertensive and aortic constricted rats. In the hypoxic control group, the capillary density was maintained despite a 20% increase in the muscle fiber diameter, indicating a proliferation of the capillary bed in proportion to the increase in muscle mass. The myocytes in all hypoxic groups were characterized by deep invaginations of the cell membrane and an increase in the number of pinocytotic vesicles. Stereological analyses of the myocytes revealed a statistically significant decrease in the mitochondria/myofibril volume ratio in animals with pressure overload. This ratio was not significantly altered when the animals were subjected to chronic hypoxia. However, there was an increase in the number of mitochondrial profiles and a decrease in the size of individual profiles in all hypoxic groups when compared to the control group.These findings suggest that cardiac hypertrophy associated with chronic hypobaric hypoxia, unlike hypertrophy due to pressure overload, is associated with a number of structural adaptations which may aid the heart in functioning in the hypoxic environment.
Article
Studies of stress-induced cardiac hypertrophy suggest that myocardial mass is regulated by the circulating level of epinephrine. The trophic effect is mediated by cardiac beta-adrenergic receptors, and in the murine, rat, and dog heart, specifically by beta2-adrenergic receptors. The well-characterized functional effects of catecholamines on heart have obscured their role as myocardial trophic hormones. Therefore, we compared the effect of beta-adrenergic receptor stimulation on the myocardial mass of both a working innervated heart and an essentially nonworking denervated heterotopically transplanted heart in the same rat; in this model, the neural and stretch parameters are nonoperational in the transplanted heart. Ornithine decarboxylase (ODC), an enzyme elevated in a dose-dependent manner in heart by isoproterenol, was assayed in both hearts to determine the relationship between ODC activity and myocardial mass in response to isoproterenol administration in workin, innervated heart compared to denervated, nonworking heart. In both recipient and donor heart, the myocardial mass paralleled the ability of an isoproterenol bolus to stimulate ODC in the respective heart. However, beta-adrenergic receptor activity in the donor heart was decreased 5 days after transplantation as assessed by the differential ability of a single dose of isoproterenol to stimulate ODC activity. Beta-receptor coupling to ODC activity in the donor heart exceeded that of the recipient heart at 10 days posttransplantation suggesting a time-dependent elevation of beta-adrenergic receptor activity in donor heart. At all times, alterations in myocardial mass paralleled beta-adrenoceptor activity as assessed by the ability of isoproterenol administration to elevate ODC activity. The results support the concept that myocardial mass is regulated by the level of circulating hormones, particularly epinephrine.
Article
The effects of exercise training were examined in the adult male rat heart using biochemical and fiber size measurements. These effects have been compared with those observed following simulated pathological cardiac enlargement associated with both moderate and severe pressure overloads. The combination of desoxycorticosterone acetate (DOCA) injections and salt loading for 21 to 25 days produced a moderate pressure overload (146 ± 5 mm Hg systolic pressure) when compared to control animals (132 ± 3 mm Hg). A 10% increase in left ventricular mass and increased fiber size accompanied the moderate pressure overload. There was no evidence for cellular proliferation in the left ventricle of DOCA injected animals. Abdominal aortic constriction for 21 to 25 days produced a severe pressure overload (210 ± 5 mm Hg) and increased left ventricular mass by 35%. There was evidence that fiber growth and cell proliferation had been stimulated. In contrast to pressure overload stimuli, 80 to 90 days of treadmill exercise did not increase left ventricular mass above control levels. There was no evidence for either increased fiber size or cellular proliferation; however, exercise established a relative left ventricular enlargement by allowing left ventricular mass to increase at approximately normal rate while simultaneously reducing the overall growth rate of the animal. The data indicate that the mechanism for achieving relative cardiac enlargement during exercise training is in direct contrast with the cardiac enlargement mechanism employed during either DOCA injection or aortic constriction.
Article
The cellular and subcellular adaptations in the myocardium of spontaneously hypertensive rats (SHR) were compared with those in Kyoto-Wistar normotensive rats with cardiac hypertrophy induced by constriction of the abdominal aorta (ACR). Hypertensive blood pressure levels were attained at eight weeks of age in SHR and coincided with the surgically-induced pressure-overload in ACR at this age. Specimens from the subepicardial and subendocardial regions of the myocardium from glutaraldehyde-perfused-fixed hearts of 16-week-old animals were compared.
Article
The effects of D,L-propranolol and its resolved epimers on cardiac size in rats given ethanol, or a control diet containing maltose-dextrin, every 8 h by gavage, for 48 h were assessed. Co-treatment with ethanol plus saline for 48 h resulted in increases of approximately 10% in wet and dry heart weights, and in their proportional measures (g/kg body wt). Cardiac protein content was increased similarly. Administration of D,L-propranolol (10, 20 mg/kg), or L-propranolol (5, 10, 20 mg/kg), suppressed the increases in response to ethanol, D-Propranolol (10, 20 mg/kg) was ineffective in attenuating ethanol-induced increases in heart weights and protein content. Values of total cardiac DNA and fractional water content were unaffected by any of the treatments. Adrenaline and noradrenaline levels in urine were elevated during 48 h of intoxication in all rats given ethanol. The results suggest that severe, subacute intoxication with ethanol induces cardiac hypertrophy. Further, the data implies that the hypertrophy is mediated through activation of cardiac beta-adrenoceptors.
Article
Noradrenaline hydrochloride (160 micrograms base/kg per h) or vehicle were infused subcutaneously for 11 days into 35 male Wistar-Furth rats using osmotic minipumps. Chronic noradrenaline infusion produced moderate hypertrophy of both ventricles without causing tissue oedema. Left ventricular (LV) hypertrophy was concentric with no change in cavity volume, increased mass: volume ratio (approximately 50%) and increased fibre diameter (approximately 25%). In the conscious rat, noradrenaline produced only a slight increase in mean arterial pressure (13%) and heart rate (11%) but a marked increase in the variability of mean blood pressure (250%). The extent of LV hypertrophy was not related to the level of mean blood pressure or to its variability. In the anaesthetized rat, peak cardiac pumping ability was normal before and after cardiac autonomic blockade. Peak pressure-generating ability during aortic occlusion was increased in hypertrophied hearts before autonomic blockade but was similar to control rats after autonomic blockade. Chronic noradrenaline administration produces cardiac hypertrophy which has many similarities to hypertensive cardiac hypertrophy but no clear association with the level of blood pressure.
Article
The weight of the heart as determined by dissection techniques was compared with liveweight and total muscle weight in different types of horses and dogs as adults and during growth. With increasing body size both within and between species, heart weight forms a lesser proportion of liveweight and of total muscle weight. Heart weight forms a greater proportion of liveweight in Thoroughbreds and Greyhounds (breeds noted for high speed running) than in other less fleet members of their species and Greyhounds have greater heart weights relative to total muscle weight than other dogs.
Article
The progression of cardiac hypertrophy and the effects on adrenal medullary catecholamine content and release were determined in rats given ethanol, in conjunction with a supplementary diet, by gavage, every eight hours for periods up to 96 hours. Ethanol caused a marked depletion of adrenal medullary adrenaline content which fell to about 25 percent of control after the full time course. During this time, there were two- to fourfold increases in urinary noradrenaline content and five- to tenfold increases in urinary adrenaline. Cardiac hypertrophy, with increases in protein content and tissue weight of both ventricles, was evident at 24 hours of intoxication. By 96 hours of treatment these markers had increased more than 20% over control values. Proportional heart weight increases per day correlated significantly with daily urinary catecholamine excretion, providing support for the hypothesis that ethanol induced cardiac hypertrophy in the rat results from catecholaminergic stimulation, primarily of adrenal medullary origin.
Article
1. The ratios between the rates of growth of the body and of the heart, kidneys, and liver are approximately uniform between 40 gm. body weight and the body weight at maturity in the albino rat. The male and female hearts grow at 0.75 times the rate of growth of the body, the male kidneys at 0.717 times, the female kidneys at 0.648 times, and the liver at 0.838 times the rate of growth of the body as a whole. 2. Formulas for the prediction of organ weight from body weight were derived from the data on 1591 albino rats kept under constant conditions. 3. A series of experiments in which dietetic and metabolic variables were introduced into otherwise constant conditions showed that the heart weight was not affected by diet, and that both kidney weight and weight of liver protein (used as a measure of effective liver size) varied in the direction of change in the protein content of the diet. Decrease in rate of metabolism induced by thyroidectomy and increase in metabolism following the administration of thyroxin led to a corresponding fall and rise of heart, kidney, and liver protein weight. These results were confirmed in experiments on fasted rats with the exception that under these conditions thyroidectomy did not appreciably decrease liver protein weight relatively to fasted controls. Increase in organ metabolism due to dinitrophenol had no effect on organ weight. 4. When experimental changes alter the composition of the body with respect to fat or water, the comparison of experimental and control organ weights in terms of any one function of body weight is fallacious. 5. Conditions that change kidney weight usually change liver protein weight in the same direction and roughly to the same degree. The possible meaning of two exceptions to this rule is discussed. 6. The observations made are regarded as supporting the hypothesis that, after weaning, change in the weight of the heart, kidney, and liver protein is determined mainly by change in the amount of work done by these organs.
A pajzsmirigy befolyisa a hypophysis szivt6megvAltoztat6 szerep6re
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  • I Hajdu
BEZNAK, M. & HAJDU, I. (1944). A pajzsmirigy befolyisa a hypophysis szivt6megvAltoztat6 szerep6re. Orvotnudomdnyi Kozlemenyek, no. 14, 1-11
Ueber den Einfluss der Schilddriise aufdie Rolle der Hypophyse in den Veranderungen der Herzmasse
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BEZiazK, M. & HAJDU, I. (1946). Ueber den Einfluss der Schilddriise aufdie Rolle der Hypophyse in den Veranderungen der Herzmasse. Schweiz. med. W8chr. 76, 390-393
Die Rolle der Hypophyse bei der Regulierung von Arbeits-vermogen und Masse des Herzens. Schweiz. med. Wschr Organ work and organ weight
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HAJDU, I. & BEZNIK, M. (1945). Die Rolle der Hypophyse bei der Regulierung von Arbeits-vermogen und Masse des Herzens. Schweiz. med. Wschr. 75, 665-669. WALTER, F. & ADDIS, T. (1939). Organ work and organ weight. J. exp. Med. 69, 467-483. ) by guest on April 17, 2012jp.physoc.orgDownloaded from J Physiol (
Experimental renal insufficiency produced by partial nephrectomy. II. Relationship of left ventricular hypertrophy, the width of cardiac muscle fibres and hypertension in the rat
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CHAIUTI, A. & BARKSDALE, E. E. (1933). Experimental renal insufficiency produced by partial nephrectomy. II. Relationship of left ventricular hypertrophy, the width of cardiac muscle fibres and hypertension in the rat. Arch. intern. Med. 52, 739-751.
A hypophysis szerepe a sziv munkakepess6g6nek es tomeg6nek szabAlyozisMban. Orvo8tudomcnyi K6zlemenyek
  • I Beznak
HAJDU, I. & BEZNAK, M. (1943). A hypophysis szerepe a sziv munkakepess6g6nek es tomeg6nek szabAlyozisMban. Orvo8tudomcnyi K6zlemenyek, no. 19, 1-23.
Die Rolle der Hypophyse bei der Regulierung von Arbeitsvermogen und Masse des Herzens
  • I Beznik
HAJDU, I. & BEZNIK, M. (1945). Die Rolle der Hypophyse bei der Regulierung von Arbeitsvermogen und Masse des Herzens. Schweiz. med. Wschr. 75, 665-669.
The effect of the adrenals and the pituitary on blood pressure and cardiac hypertrophy of rats
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BEZNkK, M. (1952b). The effect of the adrenals and the pituitary on blood pressure and cardiac hypertrophy of rats. J. Phy8iol. 116, 219-227.