Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In hypoosmolar hyponatremia, vasopressin is commonly observed to be less than maximally suppressed. This is attributed to the presence of nonosmolar vasopressin stimuli. However, the exact relationship of nonsuppressed antidiuretic hormone to specific circulatory parameters is controversial. Therefore, in the present study, we examined this question in 100 hypoosmolar hyponatremic patients in the Department of Medicine. Despite plasma hypoosmolality, vasopressin was found to be measurable in 92% of patients. Seventy patients suffered from edematous disorders (congestive heart failure, cirrhosis) or volume contraction per se; in these patients we observed unequivocal, though indirect, evidence of advanced circulatory alterations. These were associated with hyponatremia and nonsuppressed vasopressin. However, the latter could not be related directly to a specific circulatory parameter such as mean arterial blood pressure, creatinine clearance, plasma renin activity (PRA), norepinephrine, or aldosterone. However, patients with nondetectable vasopressin (n = 8) differed significantly from those with high vasopressin concentrations (n = 8: PADH greater than 9 pg/ml); in the latter, pulse rate (104 +/- 3 vs. 82 +/- 5 beats/min), plasma urea concentration (90 +/- 5 vs. 32 +/- 5 mg/dl), plasma urate concentration (7.2 +/- 0.8 vs. 3.6 +/- 0.8 mg/dl), and PRA (36 +/- 7 vs. 9.5 +/- 4.6 ng AI/ml/h) were all significantly higher than in the former. It is concluded that, in hyponatremia, the relationship between circulatory impairment and vasopressin is complex.
 ...
PMID:Vasopressin in hyponatremia: what stimuli? 243 81

In the present study, 52 patients with cirrhosis, portal hypertension, and variceal hemorrhage underwent either an elective or an emergency side-to-side portacaval shunt operation. Vasopressin was infused intravenously at 60 units/hour from just prior to abdominal incision until completion of the anastomosis. Eight of 35 patients who received vasopressin alone (23 percent) tolerated increased doses of 75 to 90 units/hour to obtain hemostasis. Four of 52 patients required simultaneous infusion of sodium nitroprusside to correct systemic hypertension. An additional 15 percent reduction in portal venous pressure occurred in these patients. Eleven of 13 patients with vasopressin-induced myocardial ischemia responded to simultaneous infusion of nitroglycerin. Further prospective studies are indicated to adequately delineate the dose and duration of therapy with either nitroprusside or nitroglycerin for simultaneous administration with intravenous vasopressin.
 ...
PMID:Simultaneous infusion of nitroglycerin and nitroprusside to offset adverse effects of vasopressin during portosystemic shunting. 249 34

Atrial natriuretic factor (ANF) is a humoral agent isolated in recent years from cardiac atrial tissue, and produced by atrial cardiocytes as a peptide precursor containing 152 amino acids. In secretory atrial granules, it is stored in reserve form as a prohormone and released into circulation as a 28-amino acid peptide from the C-terminal portion of the peptide precursor representing the active circulating hormone. ANF possesses potent natriuretic, myorelaxant, vasodilatory and blood pressure-lowering properties. Besides, it inhibits renin, aldosterone and vasopressin secretion. It is present also in the CNS and its function is closely related to the sympathetics nerves. By its direct renal and vascular effect, renin-angiotensin-aldosterone system and vasopressin inhibition and, by its neuromodulatory action on the central and sympathetic nerves, ANF plays an important role in electrolyte, volume and pressure homeostasis. The development of a radioimmunoassay for ANF determination in the plasma of rats and man enabled us to follow up its changes under various experimental conditions (water deprivation, increased or decreased salt intake, effect of anaesthetics, ontogenetic changes in ANF concentration during development of hypertension in the spontaneously hypertensive rat) and in clinical studies (effect of ECV expansion in controls, arterial hypertension, liver cirrhosis as well as ANF changes in congestive heart failure or chronic renal failure). These findings of ours have supported the concept that ANF represents an important adaptive and corrective mechanism mobilized during intravascular volume and blood pressure changes in an effort to normalize these. ANF is expected to find use also in the treatment of oedema, arterial hypertension and acute renal failure.
 ...
PMID:Atrial natriuretic factor and its role in the regulation of electrolyte, volume and pressure homeostasis. 252 70

Because the syndrome of inappropriate antidiuretic hormone (SIADH) is a state of disturbed body fluid volume regulation and altered sodium balance we sought to determine if recently described volume regulatory factors were stimulated in SIADH. We measured atrial natriuretic peptide (ANP), endogenous digitalis-like natriuretic factor (EDNF) and urinary free dopamine in SIADH (n = 27). We also determined fractional clearance of lithium (FCLi). The data obtained in SIADH were compared with similar measurements performed in sodium retaining hyponatremias, such as those of heart failure (n = 26), liver cirrhosis (n = 19) and volume contraction (n = 28). We observed: ANP was 19.5 +/- 2.7 fM/ml in SIADH; it was significantly lower than ANP in cardiac failure, but no different from ANP in volume contraction. Urinary free dopamine was 2.2 +/- 0.8 microM/24 h in SIADH; this was significantly higher than in volume contraction and liver cirrhosis. EDNF (259 +/- 42 nM/24 h) and FCLi (21.4 +/- 2%) were both numerically higher in SIADH than in other hyponatremic disorders; however, the differences did not achieve significance. In conclusion, our observations did not establish a specific role of ANP in chronic stable SIADH. As to the importance of EDNF, dopamine and proximal tubular fluid reabsorption (FCLi) additional work using acute volume changes may demonstrate their participation in the renal sodium handling of SIADH more clearly than our study did.
 ...
PMID:Natriuretic factors and lithium clearance in patients with the syndrome of inappropriate antidiuretic hormone (SIADH) 250 58

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response 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 renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, 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.
 ...
PMID:Pathophysiology of vasopressin in edematous disorders. 269 4

Remestyp Spofa is used in wide clinical practice, among others also in the comprehensive treatment of acute haemorrhage from oesophageal varices. To patients with portal hypertension, oesophageal varices associated with cirrhosis of the liver by means of an infusion pump Remestyp was administered, 13.4 micrograms/1 kg body weight for one hour. By means of a Doppler flowmeter the rate of the blood flow and the blood flow through the trunk of the portal vein was assessed before, at 10-minute intervals during infusion, and during the 90th, 120th and 150th minute. After administration of the drug no significant effect on the investigated parameters was recorded. Therefore in the same group of patients by means of a catheter before and after infusion the following parameters were assessed: central venous pressure, pressure in the pulmonary artery, cardiac minute output, pressure in the free and wedged hepatic vein. Simultaneously changes of the systemic blood pressure were investigated. After Remestyp a significant rise of the systemic blood pressure was recorded, a rise of the central venous pressure and the pressure in the pulmonary artery. The minute volume declined slightly. The pressure in the free and wedged hepatic vein rose. The authors assume therefore that the direct effect of Remestyp on the portal circulation is not haemodynamically significant. The favourable haemostyptic action of Remestyp in patients with haemorrhage from oesophageal varices is rather due to an increased tonus of the oesophageal sphincters. With regard to the very satisfactory experience with the administration of nitrates in this indication their combined administration with vasopressin or its derivatives is considered.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[The effect of terlipressin (Remestyp Spofa) on hemodynamic parameters in patients with portal hypertension associated with liver cirrhosis]. 279 Aug 79

Water retention in cirrhosis has classically been considered to be due to a low distal fluid delivery secondary to increased proximal sodium reabsorption. However, recent studies showing high plasma vasopressin levels in patients and rats with cirrhosis, ascites, and dilutional hyponatremia suggest that a nonosmotic vasopressin hypersecretion could be an alternative mechanism. To investigate the role of vasopressin in water retention in cirrhosis, the renal ability to excrete a water load (50 ml/kg body wt), as estimated by the minimum urinary osmolality and the percentage of the water load excreted during 3 h, was assessed in 10 control rats and in 20 cirrhotic rats with ascites and impaired water excretion and high urinary excretion of vasopressin. Twenty-four hours later, the same procedure was repeated in cirrhotic rats 20 min after the subcutaneous injection (30 micrograms/kg body wt) of d(CH2)5Tyr(Et) VAVP, an antagonist of the hydroosmotic effects of vasopressin (10 rats), or the vehicle (10 rats). Treatment with the vasopressin antagonist normalized water excretion in 9 of the 10 rats. No significant changes in renal water metabolism were observed in the group of rats given the vehicle. These results indicate that vasopressin hypersecretion is the predominant mechanism of the impairment in water excretion in rats with experimental cirrhosis and ascites.
 ...
PMID:Blockade of the hydroosmotic effect of vasopressin normalizes water excretion in cirrhotic rats. 279 62

The occurrence of hepatic cirrhosis with ascites and diabetes insipidus in the same patient is described. The stimulability of residual vasopressin was confirmed by water deprival and the partial vasopressin deficit by the administration of dDAVP. Water loading test referred to the possibility of suppression of residual vasopressin. Studying the specific renal functions in diets of different sodium content following the administration of dDAVP and diuretics, the diuretic without adding ADH was found to be the best therapy for these patients. Reviewing the literature the authors are taking into consideration the difficulties of differential diagnostics and the mechanisms which may explain the inhibiting effect of the liver disease on the polyuria associated with diabetes insipidus.
 ...
PMID:[Partial diabetes insipidus and ascitic liver cirrhosis in a patient]. 279 88

Bleeding from esophageal varices is a feared complication of liver cirrhosis with high mortality. Pharmacotherapy of the acute bleeding episode with vasopressin has been shown to be effective in controlled studies, but side effects of this therapy are high and therefore replacement of vasopressin with somatostatin is under investigation. Another potential lead is the combination of vasopressin with vasodilators such as nitroglycerin. While acute pharmacotherapy of the patient with esophageal varices is well accepted, chronic or prophylactic pharmacotherapy is still in the investigative stage. Prophylactic therapy with beta-blockers, e.g. propranolol, has been shown to be effective in compensated patients with alcoholic cirrhosis. In patients with more advanced stages of the disease, or with cirrhosis of other etiology, the effectiveness of propranolol has not been proven. The mechanism of propranolol is similar to that of vasopressin, i.e. it lowers portal pressure by reducing portal flow. To maintain function of the affected organ, an alternative approach--namely lowering of portal pressure through reduction of the pathologically elevated resistance--should be actively investigated.
 ...
PMID:[Pharmacological therapy of portal hypertension]. 286 82

A multicenter double-blind clinical trial was undertaken to evaluate the efficacy of a short-term somatostatin treatment versus a short-term vasopressin treatment on acute hemorrhage from esophageal varices in patients with liver cirrhosis and portal hypertension. Forty-nine patients with massive hemorrhage and endoscopic diagnosis of bleeding esophageal varices completed the study. Patients were randomly assigned to somatostatin treatment (24 patients: 250 micrograms/hr i.v. for 48 hrs) or vasopressin treatment (25 patients: 0.1 U/min i.v. for 48 hrs). The Sengstaken-Blakemore tube was utilized, when needed, for a six hour period. In case of failure the patients were crossed-over to the other treatment. Patients in whom the bleeding stopped at 48 hrs, were randomly assigned to somatostatin (250 micrograms/hr i.v.) or placebo for seven days. Bleeding stopped in 68% of patients treated with somatostatin and in 28% of patients treated with vasopressin (p less than 0.0013). Mortality rate was lower, but not significantly so, in the somatostatin group compared to the vasopressin group. No differences were noted between somatostatin and placebo in preventing bleeding recurrences. These data suggest that somatostatin, when combined if necessary with a 6 hour period of balloon tamponade, is more effective than vasopressin at low doses in controlling severe hemorrhage from esophageal varices in patients with liver cirrhosis and portal hypertension. A clinical use of somatostatin seems to be indicated in these patients.
 ...
PMID:Effect of somatostatin in controlling bleeding from esophageal varices. 288 97


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>