Article

[Pharmacological vasoconstriction in gynecology. Results obtained with ornithine-8-vasopressin]

February 1980
Rivista Italiana di Ginecologia 59(1):59-63

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PubMed

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Article

Mar 1988

In 150 patients both sides of the face underwent facelifting surgery with the local infiltration of 2% solution of ornithine 8 vasopressin which caused good surgical hemoconstriction, gave a satisfactory early postoperative period, and better results than those obtained with other solutions previously used. This series involves the use of a diluted solution compared with that usually recommended.

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Article

Diminished angiotensin-II and intact vasopressin response to hemorrhage in portal hypertension

February 1998 · Shock (Augusta, Ga.)

Portal hypertension is characterized by splanchnic vasodilation and diminished arterial vasoconstrictor response to hemorrhage. Angiotensin-II and arginine vasopressin are critical modulators of the splanchnic response to hemorrhage in normal animals. We hypothesized that alterations in endogenous renin, angiotensin-II, or arginine vasopressin production or release could contribute to the ... [Show full abstract] abnormal response to hemorrhage in portal hypertension. Hemodynamics were studied in normal and portal hypertensive rabbits following either graded isovolumetric or single large volume hemorrhage, followed by reinfusion of blood. Hemodynamic and renin-angiotensin-II, and arginine vasopressin activities were determined. The experiments demonstrated a significantly diminished appearance in angiotensin-II (110.87+/-30 vs. 245+/-51.0 pg/mL) and aldosterone (54.2+/-9.5 vs. 119.4+/-13.5 ng/dL), and plasma renin activity (19.4+/-4.2 vs. 29.1+/-2.8 ng/mL/h) in portal hypertension compared with normal, but an appropriate rise in arginine vasopressin levels following hemorrhage in portal hypertension. These findings suggest a diminished angiotensin-II production or release in portal hypertension, which may mediate the failure of the appropriate splanchnic vasoconstrictive response to hemorrhage.

Article

Recent advances in the management of hepato-renal syndrome (HRS)

February 2007 · Acta clinica Belgica. Supplementum

Hepato-renal syndrome (HRS) is a functional renal failure complicating end-stage liver disease. HRS is characterized by marked arterial vasodilation (mainly of the splanchnic bed) and severe renal vasoconstriction. HRS is classified into 2 types: type I HRS shows a rapid and progressive decline in renal function with a very poor prognosis (median survival of about 2 weeks); HRS type 2 has a more ... [Show full abstract] stable renal failure, with a median survival of about 6 months. The management of HRS is still a big challenge. The definitive therapy for HRS is liver transplantation (LT); however, the survival rate of HRS patients is poor, and important organ shortage exists. Various approaches have been used for HRS treatment including vasoconstrictor therapy. Recent evidence has shown that vasoconstrictor agents are effective and serve as a bridge to LT; the rationale for vasoconstrictors is to counteract the splanchnic arterial vasodilation and increase the effective arterial blood volume. Thus, renal perfusion and glomerular filtration rates improve. Terlipressin, a V1 vasopressin agonist, has been used frequently. A recent meta-analysis of clinical trials showed that the pooled rate of patients who reversed HRS after terlipressin therapy was 0.52 (95% CI, 0.42; 0.61; P = 0.0001, /2 = 24.6%). The pooled Odds Ratio (OR) for mortality rate in HRS patients who were not responders to terlipressin versus responders was 5.746 (95% CI, 1.5; 21.9; P = 0.0005). Prospective, controlled clinical trials are in progress to address the impact of vasoconstrictor use on survival in HRS patients. Alternative therapies such as transjugular intrahepatic portosystemic shunts (TIPS) and extracorporeal albumin dialysis (ECAD) have given encouraging results but experience is extremely limited.

Article

Effect of thyroid hormones on vascular response

October 1964 · Journal of Laboratory and Clinical Medicine

The effect of thyroid hormones on blood flow alterations produced by norepinephrine, epinephrine, angiotensin, and vasopressin has been investigated. Dogs and cats were divided into several groups according to the different thyroid preparation which they received for a period of 2 weeks. Control groups were given lactose. Heart rate, blood pressure, body weight, electrocardiogram, serum ... [Show full abstract] cholesterol, and, in some animals, oxygen consumption were recorded before and after treatment. The vasoactive drugs were infused into the femoral artery while blood flow of the hind limb was recorded by venous occlusion plethysmography both before and after thyroid administration. Contrary to expectation, both epinephrine and norepinephrine produced significantly less vasoconstriction following the administration of thyroid hormones. There was no significant alteration in the effect of angiotensin or vasopressin. Nethalide, a selective beta adrenergic blocking agent, restored vasoconstriction produced by epinephrine or norepinephrine in animals treated by thyroid preparations. It is suggested that in hyperthyroidism there may be an increased sensitivity of the beta receptors rather than a general increased sensitivity to catecholamines.

Article

The milk-ejecting effect induced by oxytocin and vasopressin during human pregnancy

August 1964 · American Journal of Obstetrics and Gynecology

Néstor L. Sala

The milk-ejecting effect induced by oxytocin and vasopressin during human pregnancy was studied by recordings of intramammary pressure. The threshold dose for response to oxytocin and vasopressin is high at the beginning of pregnancy and suffers a sudden drop at midgestation. At 20 weeks' gestation it reaches its lowest values for both hormones, remaining unchanged until the end of pregnancy. The ... [Show full abstract] slope of the dose-response relationship to oxytocin and vasopressin increases progressively throughout pregnancy, reaching its highest values at the end of gestation. The milk-ejecting effect induced by oxytocin is 40 to 50 times greater than that of vasopressin. This relationship does not vary during pregnancy.

Article

[ACTIONS OF ACTH AND LYSINE-VASOPRESSIN ON SYNTHESIS AND RELEASE OF CORTICOSTERONE IN THE RAT--STUDY...

January 1965 · Revue canadienne de biologie / éditée par l'Université de Montréal

Article

A Unifying Hypothesis of Sodium and Water Regulation in Health and Disease

December 1991 · Hypertension

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. Nonosmotic vasopressin release has been implicated in the water retention of these edematous disorders. The nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems in ... [Show full abstract] both experimental animals and in edematous patients. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin and activation of the renin-angiotensin system. These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. Neither total extracellular fluid volume nor blood volume is a determinant of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by a decrease in effective arterial blood volume (EABV) due to either a fall in cardiac output or peripheral arterial vasodilation. The acute response to a decrease in EABV involves vasoconstriction mediated by angiotensin, sympathetic mediators, and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The resultant renal vasoconstriction limits the distal tubular delivery of sodium and water, thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.

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[Measurement of portal vein blood flow by Doppler ultrasonography: pharmacological applications]

February 1993 · Gastroentérologie Clinique et Biologique

Article

Vasopressin receptor antagonists: Mechanisms of action and potential effects in heart failure

July 2006 · Cleveland Clinic Journal of Medicine

Steven R. Goldsmith

Increased arginine vasopressin (AVP) secretion in heart failure may lead to vasoconstriction, left ventricular remodeling, and water retention-actions that promote afterload, preload, and hyponatremia and thereby cause disease progression. Interfering with AVP-mediated signaling pharmacologically may be beneficial in heart failure. Selective antagonism of the vasopressin 2 (V2) receptor may ... [Show full abstract] facilitate a safe diuresis and normalize low serum sodium levels, as demonstrated in preliminary clinical trials. Pure V2 antagonism, however, may stimulate AVP secretion and enhance V1a signaling, while pure V1a receptor antagonism may lead to unwanted V2 stimulation and secondary water retention and volume expansion. Combined V1a and V2 receptor antagonism could potentially prove advantageous as a therapy for heart failure by acting synergistically to facilitate diuresis and improve hemodynamics.

Article

Mechanisms of Altered Contractile Responses to Vasopressin and Endothelin in Canine Coronary Collate...

January 1997 · Circulation

Mature coronary collateral arteries are hyperresponsive to vasopressin; in contrast, contractile responses of collaterals to endothelin are attenuated. Our goal was to determine the cellular mechanisms underlying these differences in reactivity using two sizes of canine collateral arteries isolated from hearts subjected to chronic coronary occlusion. Contractile responses to vasopressin (100 ... [Show full abstract] mmol/L) were enhanced threefold to fourfold in near-resistance (approximately 200 microns lumen diameter) and conduit (approximately 500 microns lumen diameter) collateral arteries compared with similarly sized noncollateral coronary arteries (P < .01). In contrast, contractions of both sizes of collaterals in response to endothelin (0.01 to 30 nmol/L) were smaller than responses of size-matched noncollateral arteries (P < .05). Pretreatment with either indomethacin (5 mumol/L), a cyclooxygenase inhibitor, or NG-nitro-L-arginine methyl ester (100 mumol/L), a nitric oxide synthase inhibitor, did not alter the relative responsiveness of collateral arteries to vasopressin or endothelin compared with noncollateral arteries. Vasopressin produced greater increases of intracellular free Ca2+ (measured by use of fura-2 microfluorometry and Ca(2+)-dependent 42K+ efflux) in smooth muscle of collateral arteries than in smooth muscle of noncollateral arteries (P < .05). Surprisingly, endothelin-induced increases of Ca2+ were not different in smooth muscle of collateral and noncollateral arteries (P > .05). We conclude that altered contractile responsiveness of collateral arteries to vasopressin and endothelin does not result from altered synthesis/release of nitric oxide or prostaglandins. Parallel enhancement of vasopressin-mediated Ca2+ and contractile responses suggests increases in vasopressin receptor number, affinity, and/or efficiency of coupling mechanisms in collateral smooth muscle. The dissociation between endothelin-induced contractile and Ca2+ responses of collaterals indicates that the mechanisms involved in increasing Ca2+ sensitivity of contractile proteins during endothelin stimulation may be altered in collateral arteries.

Article

[Effect of ornithine-8-vasopressin on the contractility of the uterine blood vessels in pregnant wom...

February 1971 · Ginekologia Polska

Article

Full-text available

Vasopressin in vasodilatory shock: Is the heart in danger?

February 2008 · Critical Care

In patients with hyperdynamic hemodynamics, infusing arginine vasopressin (AVP) in advanced vasodilatory shock is usually accompanied by a decrease in cardiac output and in visceral organ blood flow. Depending on the infusion rate, this vasoconstriction also reduces coronary blood flow despite an increased coronary perfusion pressure. In a porcine model of transitory myocardial ischemia-induced ... [Show full abstract] left ventricular dysfunction, Müller and colleagues now report that the AVP-related coronary vaso-constriction may impede diastolic relaxation while systolic contraction remains unaffected. Although any AVP-induced myocardial ischemia undoubtedly is a crucial safety issue, these findings need to be discussed in the context of the model design, the dosing of AVP as well as the complex direct, afterload-independent and systemic, vasoconstriction-related effects on the heart.

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Article

Heterogeneous vascular response to vasopressin: Radial artery versus forearm blood flow

January 1997 · Journal of Hypertension

Arginine vasopressin (AVP) administered intra-arterially to normal volunteers exerts a biphasic effect on forearm blood flow when the effect is extrapolated from plethysmographic measurements. To assess whether the high-dose AVP-induced increase in forearm blood flow could be confirmed when calculating blood flow from continuous radial artery diameter and flow velocity recordings obtained by ... [Show full abstract] using a high-resolution echotracking device combined with a Doppler system. Increasing doses (0.04-0.8 ng/kg per min) of AVP were infused into a brachial artery of seven normal male volunteers (aged 21-33 years). Forearm blood flow derived from venous occlusion plethysmography was assessed simultaneously with proximal radial artery blood flow calculated from luminal area and flow velocity measurements. Confirming previous reports, plethysmography showed an increase in global forearm blood flow by > 100% with AVP concentrations > or = 0.2 ng/kg per min. In contrast, direct measurements of lumen diameter and blood flow velocity in the radial artery revealed a marked dose-dependent vasoconstriction with a > 30% decline in blood flow at the highest AVP concentration. The discrepancy between the two measurements suggests that AVP has a dual effect on forearm haemodynamics. At high AVP concentration, the muscle blood flow increase predominates over the vasoconstriction in the skin circulation. Furthermore, this study strongly suggests a heterogeneity of the vascular response to vasomediators by showing that opposing responses exist not only between resistive and conduit vessels but also between conduit arteries of a common vascular bed.

[Pharmacological vasoconstriction in gynecology. Results obtained with ornithine-8-vasopressin]

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