Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of vaso-active agents on hepatic function and splanchnic oxygenation were studied in 17 patients with cirrhosis and portal hypertension. Eight patients received vasopressin (0.3 iu/min) and nine patients received nitroglycerin (50 micrograms/min). Both drugs caused a significant reduction in the portal venous pressure gradient. Vasopressin infusion significantly decreased intrinsic clearance of indocyanine green (-23%, P less than 0.01). This may be due to a decreased hepatic perfusion (-28%, P less than 0.01) and portal venous oxygenation (-15% in portal venous oxygen tension, P less than 0.05). In contrast, no changes in hepatic perfusion and portal venous oxygenation were observed after nitroglycerin infusion. Nitroglycerin did not decrease intrinsic clearance of indocyanine green. These results suggest that vasodilators, rather than vasoconstrictors, might be welcome in the treatment of patients with cirrhosis and portal hypertension.
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PMID:Effects of vaso-active agents on hepatic function and blood gases in patients with cirrhosis: a study of vasopressin and nitroglycerin. 157 96

We studied the effects of the combination of nitroglycerin and vasopressin on portohepatic hemodynamics, hepatic function, and blood gases in nine patients with cirrhosis and portal hypertension. Vasopressin infusion at a dose of 0.4 U/min caused a significant fall in portal pressure, which is evaluated by portal venous pressure gradient (-34%, p less than 0.01), associated with a decrease in hepatic perfusion (-33%, p less than 0.01) and intrinsic clearance (-20%, p less than 0.01) after 30 min. The arterial oxygenation, however, was not modified (paO2; from 73 +/- 8 to 72 +/- 7 mm Hg, NS). Nitroglycerin infusion at a dose of 100 micrograms/min was then administered for 20 min. The addition of nitroglycerin produced a further reduction in free portal venous pressure (-12%, p less than 0.01), but this was not associated with a significant improvement in both hepatic perfusion (+16%, NS) and intrinsic clearance (-7%, NS). In addition, there was a significant fall in arterial oxygenation (paO2; from 72 +/- 7 to 59 +/- 5 mm Hg, p less than 0.01). We conclude that the addition of nitroglycerin to vasopressin has a beneficial effect on free portal venous pressure, but does not have hepatic benefit. Moreover, sufficient care must be taken, when treating portal hypertension with this combination, to avoid arterial hypoxemia.
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PMID:Portohepatic pressures, hepatic function, and blood gases in the combination of nitroglycerin and vasopressin: search for additive effects in cirrhotic portal hypertension. 159 Mar 7

Bleeding from esophagogastric varices carries a high mortality rate. Active variceal bleeding can usually be temporarily controlled medically with a combination of intravenous vasopressin and nitroglycerin, with balloon tamponade, or with endoscopic sclerotherapy. Because of the high likelihood of recurrence, long-term treatment, such as repeated sclerotherapy, propranolol therapy, or shunt surgery, is necessary. The proper selection of such measures requires consideration of the site of variceal bleeding, local availability of specialized techniques, and patient factors. Only liver transplantation reverses the liver damage and offers hope of improved long-term survival. As success at identifying high-risk patients by endoscopic features improves, propranolol or other pharmacologic prophylaxis may become an acceptable treatment.
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PMID:Bleeding esophagogastric varices. Ways to treat active episodes and prevent recurrence. 167 70

The main aim of conservative treatment of upper gastrointestinal bleeding in portal hypertension is aim to treat and prevent esophageal variceal hemorrhage. Controlled trials show that the hemostasis rate following vaso-active therapy (vasopressin and analogues, somatostatin) is only slightly superior to the spontaneous hemostasis rate. Complications caused by vasopressin treatment can be avoided by concomitant application of nitroglycerin or by alternative treatment with somatostatin. Balloon tamponade is slightly superior to vasopressin for arresting variceal hemorrhage. Injection sclerotherapy influences acute bleeding most positively. Analysis of controlled trials favors sclerotherapy for prophylaxis of rebleeding, but beta-adrenoceptor blockers appear to be almost equally good.
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PMID:Conservative treatment of upper gastrointestinal bleeding in portal hypertension. 168 47

We tested the hypothesis that airway perfusion modifies the contractile response of airway smooth muscle to allergen challenge by influencing the clearance of locally released spasmogens. In six intact, lightly sedated, sheep allergic to Ascaris suum, we measured tracheal mucosal blood flow (Qtr) with a soluble gas uptake method and tracheal dead space (Vtr), an index of airway smooth muscle tone, by helium dilution before and serially after local aerosol challenge with A. suum extract or ragweed extract (control). The former challenge was repeated during continuous intravenous infusion of either vasopressin or nitroglycerin, which by themselves had no effect on Vtr and decreased and increased Qtr, respectively. Ragweed had no effect on Qtr and Vtr, whereas A. suum increased mean (+/- SE) Qtr by 111 +/- 31% (p less than 0.05) and decreased mean Vtr by 15 +/- 2% (p less than 0.05) immediately after challenge, with Qtr returning to baseline by 40 min and Vtr by 80 min. Vasopressin infusion prevented the A. suum-induced increase in Qtr and prolonged the decrease in mean Vtr (p less than 0.05). During nitroglycerin infusion, A. suum failed to alter Qtr or Vtr. Vasopressin and nitroglycerin had no effect on the contractile responses of tracheal smooth muscle to A. suum in vitro. These results indicate that the effects of vasopressin and nitroglycerin on antigen-induced airway smooth muscle contraction in vivo were due to alterations in airway blood flow rather than to alterations in the release of or airway smooth muscle responsiveness to chemical mediators.
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PMID:Airway blood flow modifies allergic airway smooth muscle contraction. 190 92

To determine whether nalbuphine might replace fentanyl as the principal opioid for anesthesia during coronary artery bypass surgery, 20 patients undergoing myocardial revascularization were anesthetized with flunitrazepam and with a continuous infusion of either nalbuphine (an opioid agonist-antagonist) or fentanyl (a pure opioid agonist) in equipotent dosage ratio of 333:1. During endotracheal intubation, all patients given nalbuphine, but only one given fentanyl (P less than 0.05), required nitroglycerin to control arterial blood pressure. Two minutes after tracheal intubation, plasma values of epinephrine, norepinephrine, vasopressin, and cortisol did not change in the fentanyl group compared with the awake (baseline) levels, whereas catecholamines and vasopressin significantly increased with nalbuphine compared with the baseline and with the values in the fentanyl group. A steady state of anesthesia (30 min after intubation), when compared with the baseline, was characterized by unchanged systemic and pulmonary blood pressures and increased systemic vascular resistance with nalbuphine, by decreased systemic and pulmonary pressures and resistances with fentanyl, and by comparably decreased cardiac index with both opioids. Hormone values returned to baseline levels but norepinephrine remained significantly higher in the nalbuphine than in the fentanyl group. A bolus injection of either nalbuphine (2.5 mg/kg) or fentanyl (7.5 micrograms/kg) given during the steady-state period of anesthesia provoked only minimal hemodynamic changes. Before skin incision, 7 of 10 patients receiving nalbuphine required nitroglycerin to control arterial blood pressure. After sternotomy, both groups required nitroglycerin, but additional antihypertensive drugs were necessary mainly in the nalbuphine group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of nalbuphine and fentanyl anesthesia for coronary artery bypass surgery. Hemodynamics, hormonal response, and postoperative respiratory depression. 195 30

There are three distinct phases during which treatment might influence the outcome in patients with portal hypertension and variceal bleeding: treatment of the active bleeding episode, the prevention of recurrent haemorrhage and perhaps most controversially the use of prophylactic therapy to avert the first bleeding episode. For the treatment of active haemorrhage injection sclerotherapy is almost certainly the treatment of choice when the expertise is available. In the absence of such, vasoconstrictor therapy continues to be widely adopted as a temporizing measure. The efficacy of vasopressin as a single agent has been limited by associated cardiovascular complications. The addition of nitroglycerin to a vasopressin regime has recently been shown to reduce such complications and to improve overall efficacy. Somatostatin represents an alternative vasoconstrictor with increasing evidence of efficacy in the absence of serious complications. Long-term injection sclerotherapy is widely accepted as the first line treatment to prevent recurrence of variceal haemorrhage although early rebleeding, prior to the obliteration of varices, represents an important limitation of therapy. Alternative local endoscopic therapy using tissue adhesives or banding of varices are under evaluation. The major claims of benefit initially attributed to oral propranolol for the prevention of rebleeding have now been considerably modified and a specific role remains to be defined. Both injection sclerotherapy and B-adreno-receptor have been proposed as prophylactic therapy to prevent the first variceal haemorrhage. Two extremely positive reports of prophylactic sclerotherapy have received little further support and there are now few protagonists of this approach.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A critical review of the medical treatment of portal hypertension. 198 46

Balloon tamponade and vasoactive drugs such as vasopressin, glypressin, vasopressin and nitroglycerin combined and somatostatin are the mainstay of noninvasive emergency treatment of bleeding gastroesophageal varices. However, their hemostatic efficacy is limited and recurrent bleeding occurs in at least one half of the patients. Survival is not improved. Unwarranted side effects and complications may be severe. Therefore, vasoactive drugs and balloon tamponade can only serve as temporizing measures until some means of definite control of bleeding such as sclerotherapy is available.
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PMID:[Immediate conservative therapeutic measures in acute variceal hemorrhage (including catheter blockage)]. 198 74

Experiments were designed to study the effects of perindoprilat (S 9780) on endothelium-dependent and -independent relaxations and contractions in isolated blood vessels. Rings of either canine femoral, basilar or left anterior descending coronary arteries, pulmonary veins, or thoracic aortas from normotensive and hypertensive rats were suspended in organ chambers for isometric tension measurement. Perindoprilat did not evoke endothelium-dependent or -independent relaxations of femoral arteries, basilar arteries, coronary arteries, or rat aortas. The compound did not affect the endothelium-independent relaxations induced by isoproterenol and nitroglycerin in canine femoral arteries. However, when given to rings of canine basilar and coronary arteries, increasing concentrations of perindoprilat potentiated the endothelium-dependent relaxation to bradykinin. In addition, the drug potentiated the endothelium-dependent relaxations to acetylcholine and thrombin in preparations of canine left anterior descending coronary arteries. In contrast, perindoprilat did not cause changes in tension when given in the presence of either adenosine diphosphate, serotonin, or arginine-vasopressin. The compound did not modify the endothelium-dependent contractions evoked by the calcium ionophore A23187 and acetylcholine in canine basilar arteries. It also did not alter endothelium-dependent contractions to arachidonic acid or to hypoxia in canine pulmonary veins or to acetylcholine in the aorta of the spontaneously hypertensive rat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of perindoprilat on endothelium-dependent relaxations and contractions in isolated blood vessels. 204 12

Previous in vivo studies have shown that vasopressin, which releases the endothelium-derived relaxing factor and constricts coronary smooth muscle, produces augmented constriction of coronary microvessels perfused by mature collaterals. We hypothesized that chronic perfusion through collaterals produces endothelial dysfunction in the recipient vasculature. Mature collaterals were stimulated in mongrel dogs by the ameroid constrictor technique. After 3-6 months, rings of conduit vessels (obtuse marginals) were studied in organ chambers, and coronary microvessels (100-220 microns) were studied in a pressurized, no-flow state with a microvessel imaging apparatus. Eleven dogs were used as controls. Large vessels were preconstricted with prostaglandin F2 alpha to 30-70% of the maximum potassium chloride tension, and microvessels were preconstricted to 20-60% of the baseline diameter with the thromboxane mimetic U46619. Relaxations to the receptor-mediated agents acetylcholine and ADP were markedly impaired in collateral-dependent coronary microvessels, whereas relaxations to nitroglycerin were enhanced compared with microvessels from control dogs. Relaxation to the calcium ionophore A23187, which releases the endothelium-derived relaxing factor through nonreceptor-mediated mechanisms, were similar in control and ameroid microvessels. Constriction to vasopressin was augmented in collateral-dependent microvessels compared with controls. Responses to all agonists were similar between control and collateral-dependent large vascular rings. In conclusion, chronic perfusion through collateral vessels selectively impairs receptor-mediated endothelium-dependent relaxations and augments constriction to vasopressin in the coronary microcirculation. These findings may have important implications regarding neurohumoral regulation of perfusion to collateral-dependent myocardium.
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PMID:Endothelial modulation of the coronary vasculature in vessels perfused via mature collaterals. 211 43


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