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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study investigated to what extent measurements of wedged and free hepatic venous pressures adequately reflect the effects of vasopressin at the esophageal varices in patients with cirrhosis. Eleven patients undergoing therapeutic sclerotherapy were studied by measuring wedged hepatic venous pressure, intravariceal pressure, free hepatic venous pressure, superior vena cava pressure and the intravascular pressure gradients wedged hepatic venous pressure-free hepatic venous pressure and intravariceal pressure-superior vena cava pressure, prior to and after vasopressin injection (1 IU, iv). Vasopressin caused a significant reduction in intravariceal pressure (from 22.5 +/- 9.4 to 19.2 +/- 8.4 mm Hg, p less than 0.001). Measurement of wedged hepatic venous pressure and free hepatic venous pressure closely reflected the reduction in variceal pressure. Thus, wedged hepatic venous pressure decreased by 16 +/- 11%, which is close to the 14 +/- 7% change in intravariceal pressure, and the 23 +/- 12% fall in the pressure gradient wedged hepatic venous pressure-free hepatic venous pressure was mirrored by the 26 +/- 10% change in intravariceal pressure-superior vena cava pressure. These pressure gradients decreased more than the absolute pressures (intravariceal pressure and wedged hepatic venous pressure) due to concomitant increases in superior vena cava pressure (1.9 +/- 1.9 mm Hg) and free hepatic venous pressure (0.6 +/- 1.9 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of vasopressin on the intravariceal pressure in patients with cirrhosis: comparison with the effects on portal pressure. 339 13

The effects of somatostatin and vasopressin on blood gases, pulmonary and systemic hemodynamics, and portal pressure assessed by the gradient between occluded and free hepatic vein pressures, were investigated in 18 patients with liver cirrhosis. In the first 10 patients, an iv bolus of 250 microgram somatostatin, followed by an infusion of 125 microgram somatostatin over 30 min, caused a sudden rise in pulmonary and systemic vascular pressures lasting 2 to 5 min and accompanied by bradycardia. There was a slight and transient increase in venous admixture (Qsp/Qt) and alveolar-arterial oxygen tension gradients (P(A-a)O2), and a transient reduction in O2 delivery (O2 del) (-11% of the baseline values) and portal pressures (-14%). In the next 8 patients, vasopressin, 0.4 U/min infused over 30 min, caused a more persistent pulmonary and systemic hypertension and bradycardia, a slight increase in P(A.a)O2 and Qsp/Qt, a reduction in O2 del (-27%) and a decrease in portal pressures (-32%). These effects were marked during the entire vasopressin infusion period. Both somatostatin and vasopressin had vasoconstrictive properties and exerted negative effects on hemodynamics and blood gases. Vasopressin appeared to be a more potent drug than somatostatin.
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PMID:Effect of vasopressin and somatostatin on hemodynamics and blood gases in patients with liver cirrhosis. 612 42

Haemorrhages in the course of cirrhosis and portal hypertension are surgical emergencies. Nevertheless medical treatment may be necessary both to revive the patient and temporarily to check the haemorrhaging itself. Some views are presented on the use of drugs, both those already in clinical use and others at the experimental stage, which appear to be effective in the treatment of haemorrhaging in portal hypertension (Vasopressin, glypressin, prostaglandin, somatostatin, propranolol, cimetidine and ranitidine).
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PMID:[Recent developments in the medical treatment of emergency cirrhotic hemorrhage. Vasopressin and glipressin, prostaglandins, somatostatin, propranolol, cimetidine and ranitidine]. 613 72

Continuous vasopressin infusion has been shown to control bleeding from oesophageal varices in patients with cirrhosis of the liver. The mortality, however, has not been changed. To investigate whether reduction of portal blood flow over a period of hours deteriorates the liver function, we measured the splanchnic blood flow and galactose and oxygen consumption in five cirrhotic patients during liver vein catheterization. Vasopressin was given as a continuous infusion of 0.2 units per min for three h. The splanchnic blood flow was reduced to 70% of control values and remained so throughout the infusion. After three h no impairment of the liver function was found. The wedged hepatic pressure (portal pressure) rose slightly, probably due to the increase of the central venous pressure reflecting impaired cardiac function. The reported beneficial effect of vasopressin on varix bleeding probably depends on the reduced portal flow per se.
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PMID:The effect of continuous vasopressin infusion on splanchnic blood flow, liver function, and portal and central venous pressures in patients with cirrhosis. 661 Feb

We have investigated the effects on systemic, pulmonary, hepatic, and renal hemodynamics, and on blood gases of vasopressin, 0.4 U/min I.V. first alone, then in combination with nitroprusside 1-5 micrograms/kg/min I.V., in 12 patients with liver cirrhosis and portal hypertension. Portal pressures were estimated by the gradient between occluded and free hepatic vein pressures, hepatic blood flow was measured by indocyanine green infusion, renal blood flow by an isotopic method, and cardiac output by thermodilution. Vasopressin alone reduced cardiac output (-23%) and O2 delivery to the tissues (-25%), increased mean arterial pressure (+20%) and filling pressures of the heart (+136%), reduced portal pressures (-36%) (from 19 +/- 1 to 12 +/- 1 mmHg, mean +/- SEM), hepatic blood flow (-35%) (1.33 +/- 0.2 to 0.87 +/- 0.1 l/min), and renal blood flow (-16%) (0.77 +/- 0.07 to 0.65 +/- 0.05 l/min). Adding nitroprusside restored cardiac output, preload and afterload, and renal blood flow to pretreatment values. Oxygen delivery remained depressed (-12%) because of a negative effect on pulmonary gas exchange (physiologic shunt increased from 16 +/- 2 to 28 +/- 4%). Portal pressures remained reduced by 31% and hepatic blood flow by 25%. These results suggest that small doses of I.V. nitroprusside minimize the deleterious hemodynamic effects of vasopressin while maintaining the therapeutic benefit of portal pressure reduction in cirrhotic patients.
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PMID:Hemodynamic effects of vasopressin, alone and in combination with nitroprusside, in patients with liver cirrhosis and portal hypertension. 669 34

To analyze the relationship between the splanchnic and systemic effects of vasopressin and to measure its efficacy in lowering portal pressure relative to what can be accomplished by zero gradient shunting, intraoperative measurements of cardiac output and relevant pressures were made in 30 patients undergoing selective or total shunts. Vasopressin caused a significant increase in systemic vascular resistance and pulmonary capillary wedge pressure, but an insignificant overall reduction in cardiac index (CI). However, in ten patients the decrease in CI exceeded 20%, suggesting a subpopulation of especially susceptible individuals. High initial CI, age, pre-existent heart disease, and severity of cirrhosis did not predict greater vulnerability. Adding an infusion of nitroprusside regularly reverted CI to control levels, regardless of the extent of cardiac output depression. Vasopressin was 38% as effective as a subsequent shunt in reducing splanchnic venous pressure. The portal hypotensive action bore no relationship to CI, but the pressure decrease caused by vasopressin was predictive of the reduction that could be achieved by shunting. The effects of the two types of shunts on systemic hemodynamics were minor and remarkably similar.
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PMID:Vasopressin and splanchnic shunting. A quantitative comparison. 707 52

Vasopressin (Pitressin) infusion through peripheral veins is a commonly used modality for control of bleeding esophageal varices. In this report we describe the development of infected gangrene at the site of accidental vasopressin infiltration in a patient with diabetes mellitus, cirrhosis and bleeding esophageal varices. Among the explanations for the development of gangrene are: 1. continuous intravenous administration; 2. diabetic peripheral vascular disease; 3. mechanical compression of extravasated fluid in a closed space. No antagonist has been clinically proven to reverse the vasoconstrictive effects of vasopressin.
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PMID:Infected gangrene. A serious complication of peripheral vasopressin administration. 741 38

The current treatment of hyponatremia is unsatisfactory and can be associated with significant morbidity. Vasopressin is inappropriately elevated in the majority of patients with hyponatremia and causes free water retention by stimulating V2-receptors in the collecting ducts. Recently, orally active, nonpeptide, selective vasopressin V2-receptor antagonists have been characterized and offer an exciting prospect for the treatment for hyponatremia. V2-receptor antagonists are effective aquaretic agents, that are capable of increasing free water clearance and plasma sodium and might be useful in the treatment of hyponatremia caused by syndrome of inappropriate secretion of antidiuretic hormone, heart failure, cirrhosis, and nephrotic syndrome. The rationale for their use and evidence from animal and human studies are discussed.
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PMID:Vasopressin V2-receptor antagonists: panaceas for hyponatremia? 932 5

Hepatorenal syndrome is a frequent complication associated with extremely short survival in cirrhotic patients with alcoholic hepatitis. Vasopressin analogs have been reported to induce transient regression of hepatorenal syndrome in patients with cirrhosis. However, treatment withdrawal was followed by early recurrences in every case. We report the case of a 68-yr-old woman with severe alcoholic hepatitis complicated by hepatorenal syndrome. Terlipressin induced a prolonged recovery of renal function that was associated with improvement in hepatic function.
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PMID:Terlipressin may influence the outcome of hepatorenal syndrome complicating alcoholic hepatitis. 936 5

Vasopressin (AVP) is released in response to both osmotic and nonosmotic stimuli. Nonosmotic-stimulated AVP release occurs in cardiac failure, cirrhosis, and pregnancy in response to alterations in arterial circulatory integrity. Cardiac failure in rats is associated with increased plasma AVP and hypothalamic AVP mRNA, and in humans, it is associated with cardiac failure. Plasma AVP concentrations are elevated when measured with a sensitive radioimmunoassay. Urinary concentrations of AVP-responsive aquaporin-2 water channels are also elevated in cardiac failure. V2 receptor antagonists correct the impaired solute-free water excretion seen in rats with low-output cardiac failure and reverse the upregulation of renal aquaporin-2 water channels. Orally active non-peptide-selective V2 receptor antagonists administered to patients with congestive cardiac failure decrease urinary concentrations of aquaporin-2, increase solute-free water clearance, and correct the hyponatremia. Cirrhosis of the liver results in splanchnic arterial vasodilation and increased vascular capacity, most likely secondary to increased nitric oxide production. This relative underfilling of the arterial circulation stimulates nonosmotic AVP release with resultant water retention. Aquaporin-2 gene expression is upregulated in the kidneys of rats with cirrhosis of the liver. AVP-2 receptor antagonists administered to animals with cirrhosis reverse the water retention. Human studies using orally active, non-peptide-selective V2 receptor antagonists in patients with cirrhosis are currently underway. Pregnancy is another state of nitric oxide-mediated arterial vasodilation that is associated with plasma AVP concentrations that are relatively high for the degree of hypoosmolality. Upregulation of the water channel aquaporin-2 in the renal papillae of pregnant rats has also been demonstrated, and this effect is reversed by administration of a V2 receptor antagonist.
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PMID:Vasopressin release, water channels, and vasopressin antagonism in cardiac failure, cirrhosis, and pregnancy. 975 91


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