Cardioscience (Cardioscience)

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ISSN 1015-5007
OCLC 22106908
Material type Periodical
Document type Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Many studies have shown that the contractile response of the rat left ventricle is impaired in diabetes mellitus. Few studies have examined the acute in vivo effects of catecholamines on the right ventricle of diabetic rats. The present study investigates the acute in vivo effects of norepinephrine (100 continuous intravenous infusion for 15 minutes) on the function of the right and left ventricle of diabetic rats. The effects of isoproterenol (25, subcutaneously) on the activity of glucose-6-phosphate dehydrogenase, the first and rate limiting enzyme of the oxidative pentose phosphate pathway, and on adenine nucleotide biosynthesis of the diabetic heart were also examined. Diabetes mellitus was induced by a single intravenous injection of streptozotocin (60 4 weeks before measurements. The hemodynamic measurements were made on intact, anesthetized rats with Millard ultraminiature pressure tip catheters. The basal hemodynamic measurements (left ventricular systolic pressure, diastolic aortic pressure, left ventricular dP/dtmax, right ventricular systolic pressure and right ventricular dP/dtmax) as well as glucose-6-phosphate dehydrogenase activity and adenine nucleotide biosynthesis were the same in the diabetic animals as in the controls. Heart rate was slower in the diabetics. Norepinephrine, after 15 minutes of intravenous infusion, induced a marked increase in heart rate, left ventricular dP/dtmax, right ventricular systolic pressure and right ventricular dP/dtmax; whereas left ventricular systolic pressure and diastolic aortic pressure remained unchanged. Isoproterenol caused a pronounced stimulation of both cardiac glucose-6-phosphate dehydrogenase activity (after 24 hours) and adenine nucleotide biosynthesis (after 5 hours).(ABSTRACT TRUNCATED AT 250 WORDS)
    Cardioscience 07/1995; 6(2):131-8.
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    ABSTRACT: We have investigated the incorporation of cholesterol oxidation products into cardiomyocyte lipids and related this to changes in cell proliferation, evaluated by measuring cellular protein content. Primary cultures of neonatal rat ventricular cells were supplemented with scalar concentrations of several cholesterol oxidation products (cholestan-5 alpha, 6 alpha-epoxy-3 beta-ol, 5 alpha-cholestane-3 beta, 5, 6 beta-triol, 5-cholesten-3 beta, 4 beta-diol, 5-cholesten-3 beta-ol-7-one, and 5-cholesten-3-one). Although all the cholesterol oxidation products were incorporated into the cardiomyocyte lipids when added to the medium at a concentration higher than 0.5 microM, the extent of the incorporation of the different cholesterol oxidation products differed, depending on the concentration in the culture medium and on the chemical structure of the compound. The effects of the cholesterol oxidation products on the cellular protein content were also different: 5 alpha-cholestane-3 beta, 5, 6 beta-triol was shown to be the most potent inhibitor of cell proliferation, followed by cholestan-5 alpha, 6 alpha-epoxy-3 beta-ol, 5-cholesten-3 beta, 4 beta-diol and 5-cholesten-3 beta-ol-7-one. 5-Cholesten-3-one did not affect the cellular protein content. The ability of cholesterol oxidation products to inhibit cell proliferation, and their capacity to increase the permeability of the plasma membrane to calcium, could be deleterious for cardiac cells.
    Cardioscience 07/1995; 6(2):107-13.
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    ABSTRACT: The distribution of binding sites for substance P labeled with [125I]-Bolton-Hunter-reagent was studied in a mixed cell culture preparation from newborn guinea-pig atria and interatrial septum. A relatively small subpopulation of intracardiac neurons expressed substance P binding sites. These neurons exhibited a range of densities of labeling and could be heavily, moderately or lightly labeled with autoradiographic grains. In most cases, the autoradiographic grains were restricted to the neuronal cell body and more proximal regions of the neurites in culture. Intracardiac neurons expressing substance P binding sites were seen in close association with unlabeled neurons. The density of labeling and the distribution of autoradiographic grains over individual intracardiac neurons did not appear to be related to whether they were mono- or binucleate or their associated cell types. The possibility that the substance P binding sites demonstrated here represent functional receptors on intracardiac neurons and their potential role in the heart is discussed.
    Cardioscience 07/1995; 6(2):157-63.
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    ABSTRACT: To determine the effects of chronic constriction of the left coronary artery on the function and structure of the heart, coronary artery narrowing was surgically induced in rats and ventricular pump performance, extent and distribution of myocardial damage, and the hypertrophic and hyperplastic response of myocytes were examined. Alterations in cardiac hemodynamics were found in all rats, but the characteristics of the physiological properties of the heart allowed a separation of the animals into two groups which exhibited left ventricular dysfunction and failure, respectively. Left ventricular hypertrophy occurred in both groups and was characterized by ventricular dilatation and wall thinning which were more severe in the failing animals. Multiple foci of myocardial damage across the wall were seen in all animals but tissue injury was more prominent in the endomyocardium and in failing rats. The anatomical and hemodynamic changes resulted in a significant increase in diastolic wall stress which paralleled the depression in ventricular performance. Myocyte cell loss and myocyte cellular hypertrophy were more severe with ventricular failure than with dysfunction. Finally, diastolic overload appeared to be coupled with activation of the DNA synthetic machinery of myocytes and nuclear mitotic division. In conclusion, a fixed lesion of the left coronary artery leads to abnormalities in cardiac dynamics with marked increases in diastolic wall stress and extensive ventricular remodeling in spite of compensatory myocyte cellular hypertrophy and hyperplasia in the remaining viable tissue.
    Cardioscience 07/1995; 6(2):89-100.
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    ABSTRACT: The aims of this study were to develop a model of left ventricular hypertrophy in the guinea pig using the technique of aortic banding below the level of the renal arteries, and to characterize any cardiac electrophysiological changes induced. Female guinea-pigs were either sham operated or the abdominal aorta was partially occluded by banding around a 23 or 25 G needle. Following recovery, animals were monitored for 10 weeks. The left ventricular dry weight to body weight ratio was similar in sham (0.326 +/- 0.01 mg/g, n = 12) and aortic banded guinea pigs (0.308 +/- 0.1 mg/g, n = 11). Conscious mean arterial blood pressure was also not modified by the aortic banding 10 weeks after operation (72 +/- 16 (sham) vs 71 +/- 1 mmHg). The action potential characteristics measured in isolated superfused left papillary muscle stimulated at 1 Hz were similar in sham and aortic banded groups. The action potential duration measured at 50 and 90% of repolarization tended to be longer in muscle from aortic banded (122.4 +/- 10 ms ADP50 and 155.2 +/- 9.5 ms APD90) than sham operated animals (105.8 +/- 8.4 and 142.2 +/- 6.2 ms) but these differences were not statistically significant. Hypoxia abbreviated the cardiac action potential to a similar degree in muscle from sham and aortic banded animals. It is concluded that sub-renal aortic banding with a 23 or 25G needle fails to develop left ventricular hypertrophy in the guinea pig 10 weeks after operation.
    Cardioscience 07/1995; 6(2):115-9.
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    ABSTRACT: Previous studies in anesthetized animals showed that distension of the stomach or the descending colon primarily caused decreases in mean coronary blood flow. Whether these responses occurred during systole or diastole was not investigated. The present work was planned to study the primary effects of the distension of the two viscera on phasic coronary blood flow in the anesthetized pig. In ten animals, the stomach and the descending colon were distended at constant volume by injecting warm Ringer solution into intravisceral balloons (0.8 and 0.25 l respectively) while preventing changes in heart rate and arterial blood pressure. Distensions of the stomach or the descending colon caused a decrease in mean coronary blood flow in each pig. However, the decrease elicited by gastric distension occurred only during diastole, while the decrease caused by descending colon distension involved both systolic and diastolic coronary blood flows. The same effects on phasic coronary blood flow were observed during experiments in which the decreases in mean coronary blood flow elicited by distension of the stomach or the descending colon were further augmented by adding the distension of the second viscerum. The results indicate that the coronary vasoconstriction caused by gastric distension mainly involves the vessels which supply the subendocardial layers of the myocardium, while that caused by descending colon distension also involves the vessels which supply the subepicardial layers. The vasoconstrictor effect on the subendocardial coronary circulation is enhanced by the combined distension of the two viscera.
    Cardioscience 07/1995; 6(2):121-30.

  • Cardioscience 07/1995; 6(2):81-7.
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    ABSTRACT: The aim of the present study was to investigate stable left ventricular dysfunction resulting from severe myocardial ischemia in conscious dogs, in order to evaluate the action of cardiotonic agents under pathological conditions mimicking moderate cardiac failure. Mongrel dogs with a catheter implanted in the left ventricle were trained on a treadmill and subjected to a standardized exercise before and after a Harris-type ligation of the anterior descending branch of the left coronary artery in two stages. Two weeks later the lower third of the left circumflex coronary branch was also occluded, and the exercise test repeated for at least two additional weeks to evaluate the changes in the left ventricular function indicated by left ventricular systolic pressure, end-diastolic pressure, heart rate, positive and negative dP/dtmax and dP/dt/P. Noninvasive radionuclide investigations of the left ventricular function and myocardial perfusion were done before and after the development of cardiac failure. Following occlusion of the anterior descending and circumflex coronary arteries, the baseline end-diastolic pressure increased from 7.6 +/- 2.3 mmHg to 23.3 +/- 3.0 mmHg (p < 0.05) and increased even further during exercise (to 49.2 +/- 3.5 mmHg, p < 0.05). After the development of cardiac failure, no substantial change occurred in the end-diastolic pressure, either during rest or repeated exercise tests.(ABSTRACT TRUNCATED AT 250 WORDS)
    Cardioscience 06/1995; 6(2):147-55.
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    ABSTRACT: We have compared the contractile responses of the isovolumic hearts of rat and guinea pig to a rise in the coronary perfusion pressure in the range 60-120 mmHg (Gregg's phenomenon). Left ventricular systolic pressure was lower in guinea pig hearts than in rat hearts at a low coronary perfusion pressure and increased markedly less at a higher perfusion pressure, despite a greater increase in coronary flow. The rise in left ventricular systolic pressure in the guinea pig hearts was entirely due to an increased left ventricular end-diastolic pressure, while left ventricular developed pressure did not increase. The wet weight of the hearts in situ was similar in both species, but after perfusion the guinea pig hearts gained significantly more fluid than the rat hearts (65% of the initial heart weight compared to 37%). The group of rat hearts perfused with a low external concentration of Ca2+ developed a similar left ventricular pressure to the guinea pig hearts and gained a similar amount of fluid (63%), but Gregg's phenomenon was the same as in rat hearts perfused with a normal concentration of Ca2+. The results suggest that the weak Gregg's phenomenon seen in guinea pig hearts can be attributed to factors other than myocardial edema and a lower left ventricular systolic pressure.
    Cardioscience 04/1995; 6(1):25-30.
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    ABSTRACT: The purpose of this study was to evaluate changes in the proton nuclear magnetic resonance relaxation times (T1 and T2) after chronic infarction in the rat. Ligation of the left coronary artery was followed by various degrees of reduction in myocardial blood flow. The ligation induced infarction in the left ventricle and compensatory hypertrophy in the right ventricle, as evaluated by the ratio of right ventricle to body weight. The interventricular septum and the right ventricle did not become ischemic in this model and served as control areas. In the infarcted left ventricle our results showed an increase in the T1 and T2 relaxation times after 15 and 30 days of ligation and a slight decrease after 60 days. A similar change in the T1 values was observed in the right ventricle. In contrast, a persistent increase in the T2 relaxation times was observed in the right ventricle and correlated with the ratio of right ventricle to body weight (r = 0.54, p < 0.01). The observation that the magnetic resonance relaxation times in vitro are modified in the hypertrophic right ventricle after myocardial infarction could be important in interpreting magnetic resonance imaging in vivo. There was no relation between the changes in the relaxation times and the degree of myocardial ischemia.
    Cardioscience 04/1995; 6(1):39-45.
  • Z Su · Q Ling · Z G Guo ·
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    ABSTRACT: To elucidate the vascular actions of lysophosphatidylcholine, we examined its effects on the concentration of cytosolic free calcium ([Ca2+]i), plasma membrane fluidity and release of lactate dehydrogenase in vascular endothelial cells cultured from bovine aortas. The [Ca2+]i of the endothelial cells was measured by a dual-wavelength fluorospectrophotometer using a fluorescent, calcium-specific indicator, Fura-2. Membrane fluidity was monitored by measuring changes in the steady-state fluorescence anisotropies, using 1,6-diphenyl-1,3,5-hexatriene as a fluorescence probe. In the presence of 1 mmol/L extracellular calcium, lysophosphatidylcholine caused a biphasic elevation of [Ca2+]i in Fura-2-loaded vascular endothelial cells, consisting of a large transient component followed by a relatively low, but more sustained component. At concentrations of lysophosphatidylcholine equal to or greater than 10 mumol/L, [Ca2+]i increased in a dose-dependent manner in the presence or absence of external calcium. In the absence of extracellular calcium, only an initial transient increment in the [Ca2+]i of endothelial cells was generated, the sustained component being eliminated. The sustained component was greatly depressed or almost abolished by the addition of the calcium influx blocker, NiCl2. Plasma membrane fluidity was greatly increased by incubation with lysophosphatidylcholine (30 and 50 mumol/L) concomitant with significant increases in the release of lactate dehydrogenase from the cells. At 50 mumol/L, lysophosphatidylcholine increased lactate dehydrogenase release and membrane fluidity in a time-related way.(ABSTRACT TRUNCATED AT 250 WORDS)
    Cardioscience 04/1995; 6(1):31-7.
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    ABSTRACT: We have examined four models of experimental cardiac hypertrophy and heart failure for alterations in troponin isoform expression, particularly in the re-expression of the fetal isoforms. Cardiac protein extracts from experimental and sham-operated control rats were analyzed using one dimensional gel electrophoresis, followed by Western blotting and detection with antibodies specific for troponin I and T. No alteration in protein profile was observed for these proteins between control, hypertrophied and failing heart samples. The data demonstrate that reversion to the fetal pattern of troponin expression is not a feature of experimental cardiac hypertrophy and heart failure in the rat.
    Cardioscience 04/1995; 6(1):65-70.
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    ABSTRACT: The aim of the study was to examine whether stimulation of alpha- and beta-adrenergic receptors in intact rats induces cardiac hypertrophy and to characterize the metabolic alterations that precede or accompany the process of hypertrophy. Cardiac beta-adrenergic receptors were stimulated with a single subcutaneous injection of 25 mg/kg isoproterenol. This led to an increase in the cardiac cAMP level which was followed by the sequential enhancement of adenine nucleotide biosynthesis and protein synthesis. The increase in adenine nucleotide and protein synthesis induced by isoproterenol was prevented by propranolol (50 mg/kg) within the first 5 hours. Norepinephrine, given as a continuous intravenous infusion of 0.2 mg/kg for 3 days, induced an increase in heart rate, mean aortic pressure and total peripheral resistance. Cardiac output was slightly reduced. The cardiac RNA/DNA ratio and the left ventricular weight/body weight ratio were significantly increased by about 40%. Simultaneous intravenous administration of the alpha-receptor blocker prazosin (0.1 mg/kg/h) and of the beta-receptor blocker metoprolol (1 mg/kg/h) reversed the functional changes and attenuated the increase in the RNA/DNA ratio induced by norepinephrine. The left ventricular weight/body weight ratio was within the range of the control values. Selective stimulation of alpha-adrenergic receptors by continuous intravenous infusion of norfenephrine (2 mg/kg/h) for 3 days increased heart rate and total peripheral resistance, while cardiac output was significantly lower. The RNA/DNA and left ventricular weight/body weight ratios were increased. Prazosin attenuated the increase in the RNA/DNA ratio induced by norfenephrine and prevented the development of cardiac hypertrophy. In the isolated perfused working rat heart, norepinephrine (3 x 10(-8) M) increased the expression of the proto-oncogenes c-fos and c-myc after 30 and 60 minutes, respectively. This increase occurred at about the same time as that induced by volume overload (increase of preload from 8 to 16 cm H2O) and pressure overload (increase of afterload from 80 to 100 cm H2O), but was more pronounced. In intact rats, norepinephrine elicited an increase in the mRNA and activity of glucose-6-phosphate dehydrogenase, the first and regulating enzyme of the oxidative pentose phosphate pathway, in a time-dependent manner. It is suggested that this may be part of a long-term homeostatic mechanism to keep the cardiac adenine nucleotide level in the normal range.
    Cardioscience 04/1995; 6(1):47-57.
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    ABSTRACT: Treatment with propionyl-L-carnitine has been shown to increase the walking capacity of patients with peripheral vascular disease, but the mechanisms responsible for the effect are unknown. To study the effects of propionyl-L-carnitine on musculocutaneous vascular beds and the related mechanisms, a preparation of constant-pressure blood-perfused dog hind-limb was used. Since the propionyl-L-carnitine solution had a pH less than 4 the contralateral limb simultaneously received acidified saline. The substances were injected into the perfused arteries in 2 minutes or in 20 minutes, and the cumulative dose of propionyl-L-carnitine was 20 mg/kg for each administration. The preparation was well suited for this study, because there were no major systemic effects of propionyl-L-carnitine, nor signs of cross-circulation between the isolated limbs. Propionyl-L-carnitine increased flow by 130% in 2 minute infusions and by 49% in 20 minute infusions. Acidified saline increased flow by 47% in 2 minute infusions and by 34% in 20 minute infusions. The difference between propionyl-L-carnitine and acidified saline was significant in 2 minute infusions. The 2 minute infusions of propionyl-L-carnitine increased venous PO2 by 34% and PCO2 by 22% while pH decreased by 0.07. The 20 minute infusions of propionyl-L-carnitine increased PO2 by 22% and PCO2 by 24% while pH decreased 0.10 units. Acidified saline increased only venous PO2 in 2 minute infusions (16%). Calculated oxygen consumption of the perfused limbs increased in 2 minute infusions of propionyl-L-carnitine, but not significantly. It was concluded that propionyl-L-carnitine has a direct vasodilator effect in musculocutaneous vascular beds at high doses and probably enhances tissue metabolism.
    Cardioscience 04/1995; 6(1):59-64.
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    ABSTRACT: A review of the birth locus and the first developmental stages of cardiomyocytes and Purkinje cells in the chick embryo is presented in the light of recent experimental results. Experiments done in vitro have shown that the stage of 2 somites is an important morphogenetic phase, characterized by mutual identification, selective adhesion and spatial organization of the putative cardiac cells of the splanchnopleural sheet in the cardiogenic area. Many experimental data suggest that the neural crest cells moving through the corridor of the dorsal mesocardium, as well as the cholinergic system related to them, may play a role of myogenic inductors on the mesothelial putative cardiac cells. In addition, other experimental findings suggest that the Purkinje cells of the conduction system may have a crestal origin. This hypothesis is well grounded, although the origin of Purkinje cells remains to be clarified.
    Cardioscience 04/1995; 6(1):19-23.
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    ABSTRACT: The cardiovascular beneficial effects of fish oils are currently attributed to docosahexaenoic (C22:6 n-3) and eicosapentaenoic (C20:5 n-3) acids, although most investigations have focused on eicosapentaenoic acid. This study was devoted to the specific effect of docosahexaenoic acid, as compared to eicosapentaenoic acid, on the basal electrophysiological and mechanical characteristics of cultured rat myocardial cells. The myocyte cultures were prepared from newborn rat heart ventricles. The cells were grown for 24 hours in a conventional seric medium, and then incubated in a medium enriched with either docosahexaenoic acid or eicosapentaenoic acid for 96 hours. This treatment resulted in docosahexaenoic acid-rich cells (16% of the phospholipid fatty acids) and docosahexaenoic acid-poor cells (1.5%), both displaying the same phospholipid n-6/n-3 polyunsaturated fatty acid ratio. The transmembrane potentials were recorded with glass microelectrodes. Contractions were monitored photometrically. The action potential amplitude was slightly smaller in docosahexaenoic acid-rich cells (-4 mv), due to a lower plateau phase. There was no difference in action potential duration and spontaneous rate. The contraction measurements were not significantly different between the two groups of cells. We conclude that increasing the docosahexaenoic acid content in cardiomyocyte membrane phospholipids may have modulated the calcium ionic channels governing the plateau phase of the action potential, whereas the other physiological activities remained unaffected.
    Cardioscience 04/1995; 6(1):71-8.
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    ABSTRACT: The mean coronary blood flow increases in response to an increase in myocardial oxygen consumption. Conversely, an increase in coronary perfusion is itself reported to induce an increase in myocardial oxygen consumption. Such an effect can be explained by stretching of the myocardial fibers surrounding the vessels, which become more distended with an increase in perfusion. The flow in the left descending and circumflex coronary arteries is reduced in systole because of the compression exerted by the contracting myocardium on the intramyocardial vessels. Due to the thinner wall of the right ventricle, this reduction is not obvious in the right coronary artery. The intramyocardial pump model provides a satisfactory explanation of the mechanism by which contraction reduces the flow. It also explains the attenuation of the diastolic-systolic oscillations of flow which occurs in the presence of a stenosis of a large epicardial artery. The varying elastance model shows the dependence of the extent of the reduction of the flow in systole on myocardial contractile force rather than on the pressure developed in the ventricle by the contraction. However, although the ventricular systolic pressure does not affect the flow in hearts with a relatively thick wall, it contributes to the systolic reduction of flow in hearts with a relatively thin wall. Owing to a mechanism involving the coronary capacitance, contraction is also responsible for the level of coronary flow in diastole.
    Cardioscience 04/1995; 6(1):13-7.

  • Cardioscience 04/1995; 6(1):1-11.