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

The potent diuretic and natriuretic properties of atrial natriuretic factor (ANF) suggest that atrial hormones may participate to the regulation of salt and water excretion under physiological conditions. ANF, via the increase of its intracellular second messenger cGMP, has been recently shown to inhibit the apical sodium channel of the inner medullary collecting tubule (IMCD). In addition, ANF inhibits renin and aldosterone synthesis and antagonizes the antinatriuretic effects of angiotensin II. ANF may also contribute to the excretion of free water by inhibiting both the secretion of vasopressin and its antidiuretic action. ANF appears to play an important physiological role in sodium repleted states, or when the effective plasma volume is increased. On the contrary, when the effective plasma volume is decreased or in sodium depleted states, the natriuretic effect of both endogenous and exogenous ANF is severely blunted. That ANF-resistance may be related to the activation of the renin-angiotensin-aldosterone axis, increased circulating catecholamines, renal sympathetic nerve stimulation, changes in renal hemodynamics or increased degradation of ANF. All these factors could explain the lack of significant natriuretic effect of both endogenous and exogenous ANF in some pathological conditions such as heart failure or liver cirrhosis. ANF may also been concerned in water homeostasis. In addition to the well-known osmoregulatory pathways of water metabolism, we recently found that ANF could be involved in the volume adjustment to acute water intake in normal man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor and the endocrine control of electrolyte homeostasis. 183 42

Cardiac atria and, under certain circumstances, also ventricles produce and secrete into the circulation atrial natriuretic factor (ANF). ANF exerts a significantly natriuretic, myorelaxant, renin-, aldosterone-, and vasopressin-inhibiting effect and acts as a neurotransmitter in the central and autonomous nervous systems. Expansion of the extracellular volume stimulates secretion of ANF which consequently contributes to renal excretion of sodium and water. The renal effect of ANF is apparently modulated by interaction with other mechanisms. ANF concentration in peripheral blood is the product of its secretion by the heart and degradation by peripheral tissues. In ascitic liver cirrhosis, the decreased splanchnic bed uptake may contribute to the increase in plasma ANF concentration observed. Insufficient production or secretion of ANF are not likely to be the primary etiopathogenic mechanism of arterial hypertension. In the course of development of hypertension, ANF is mobilized as a corrective-adaptive mechanism in an effort to normalize the raised BP, extracellular volume or circulating pressor agents. Through its production of ANF, the heart possess an important endocrine function markedly affecting pressure, electrolyte and volume homeostasis.
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PMID:Role of the heart as an endocrine organ. 184 37

In patients with portal hypertension, bleeding from the gastric mucosa is common, and is often treated with vasopressin (VP). VP reduces the portal pressure by contracting the arterioles of the abdominal organs. In normal rats, VP reduces the gastric mucosal blood flow (GMBF). However, it is not sure whether the reduction of the portal pressure by VP actually reduces the GMBF in patients with portal hypertension. Here, we studied the effects of VP on the GMBF of 24 patients with portal hypertension resulting from cirrhosis. The ICG15 test was done for 20 of the patients. We measured the GMBF of the antrum and body of the stomach using a laser Doppler flowmeter (Peliflux PF 2) connected with a gastrofiberscope without VP on one day and about 10 min after the start of administration of VP (0.4 U/min, i.v.) on another day. Unexpectedly, the GMBF was increased with VP in 14 of 22 patients at the antrum and in 19 of 24 patients at the body of the stomach. In the body of the stomach, there was correlation between the increase in the GMBF caused by VP and the results of the ICG15 test. A high ICG15 reflects high portal pressure, so this finding indicates that in high portal pressure, the GMBF is increased by VP, and in low portal pressure, the GMBF is decreased by VP.
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PMID:Effects of vasopressin on gastric mucosal blood flow in portal hypertension. 188 71

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 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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PMID:Unifying hypothesis of sodium and water regulation in health and disease. 193 81

Endogenous opioids may be involved in the pathogenesis of ascites and edema in patients with liver cirrhosis. We administered the opioid antagonist naloxone (5 mg bolus followed by a 0.06 mg/min infusion) to eight male patients with alcoholic cirrhosis and ascites and to five healthy age- and sex-matched control subjects and determined the effects of naloxone on water and electrolyte excretion after a nonsustained water load (20 ml/kg). In comparison with saline vehicle infusion carried out in the same subjects, naloxone administration resulted in a 50% increase in urine output and creatinine clearance and twofold increases in sodium and potassium excretion in patients with cirrhosis. Fractional sodium and potassium excretion, minimal urinary osmolality, plasma vasopressin and aldosterone levels, arterial blood pressure, and heart rate were not affected by naloxone treatment. The diuretic effect of naloxone was not observed in control subjects. Plasma naloxone levels were about six times higher in patients with cirrhosis than in control subjects (probably because of impaired metabolism of the drug) but only a weak correlation was found between drug levels and the degree of diuresis observed. The diuretic effect of naloxone may be related to an increase in glomerular filtration rate, possibly in conjunction with altered tubular reabsorption.
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PMID:Naloxone increases water and electrolyte excretion after water loading in patients with cirrhosis and ascites. 194 May 89

Somatostatin (ST) and vasopressin (VP) infusions were compared in the treatment of actively bleeding esophageal varices. Fifty-four patients with liver cirrhosis were included in the study. Thirty-two were given ST 4.2 micrograms/min, and 22 patients were given VP 0.4 IU/min for 72 h after endoscopic diagnosis. The role of alcoholic cirrhosis was similar in both groups. Initial control of bleeding was achieved significantly more often (p = 0.0281) when ST was used (84.4%) than during VP treatment (57.1%). Rebleeding occurred in 18.8% and 4.8%, respectively. Side effects of treatment were significantly more common when VP was used than during ST treatment (p = 0.0021). Overall mortality was high in both groups, being 34% in the ST group and 36% in the VP group. ST infusion seems to be more effective and safer than VP in the treatment of acute variceal bleeding. However, the high frequency of rebleeding during ST treatment means that, after primary hemostasis with ST infusion, other methods, such as surgery or sclerotherapy, are needed to prevent the serious complications of rebleeding.
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PMID:Comparison of somatostatin and vasopressin in bleeding esophageal varices. 197 91

A patient is described who developed liver cirrhosis and variceal bleeding. After a continuous infusion of vasopressin rabdomyolysis occurred. Recovery of the clinical picture and of the muscle enzymes occurred 48 hours after cessation of therapy.
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PMID:[Muscular necrosis following administration of vasopressin]. 205 19

A continuous IV infusion of vasopressin was administrated to a patient with cirrhosis of the liver and acute gastrointestinal bleeding from esophageal varices. In the first 24 hours, the patient developed rhabdomyolysis and cutaneous necrosis. Stopping vasopressin infusion resulted in relief of these lesions. The rarity of these complications suggests an idiosyncratic reaction of susceptible individuals that may be related to previous vascular disease or a failure in baroreceptor regulation.
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PMID:Rhabdomyolysis and cutaneous necrosis following intravenous vasopressin infusion. 206 28

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 man, it has been found that the nonosmotic release of vasopressin is consistently associated with the 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 in the 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.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A unifying hypothesis of sodium and water regulation in health and disease. 210 96

We measured the haemodynamic changes following triglycyllysine vasopressin administration and after addition of nitroglycerin in twelve patients with portal hypertension due to hepatitis B-related cirrhosis. A bolus i.v. injection of triglycyllysine vasopressin at a dose of 2 mg reduced the hepatic venous pressure gradient from 18.5 +/- 3.7 (mean +/- S.D.) to 15.6 +/- 4.0 mmHg, p less than 0.001. However, the cardiac index decreased from 4.8 +/- 1.0 to 3.7 +/- 0.8 l/min m2, p less than 0.001; the heart rate decreased from 79 +/- 15 to 71 +/- 13, p less than 0.01; the right atrial pressure increased from 3.2 +/- 1.9 to 5.3 +/- 2.3 mmHg, p less than 0.001; the mean arterial pressure increased from 92 +/- 13 to 103 +/- 13 mmHg, p less than 0.05; and the systemic vascular resistance rose from 939 +/- 182 to 1367 +/- 310 dyn/s cm-5, p less than 0.001. Furthermore, both mean pulmonary arterial pressure and pulmonary capillary wedge pressure showed a significant increase following triglycyllysine vasopressin administration as compared with baseline values (p less than 0.005). The addition of sublingual nitroglycerin at a dose of 0.6 mg returned all the systemic haemodynamic parameters to baseline levels. On the other hand, nitroglycerin administration caused no further change in the hepatic venous pressure gradient. We concluded that although triglycyllysine vasopressin significantly reduced portal pressure in patients with hepatitis B-related cirrhosis, it produced untoward systemic haemodynamic changes similar to those seen with vasopressin. The addition of nitroglycerin improved the detrimental systemic haemodynamic effects produced by triglycyllysine vasopressin without further reducing the hepatic venous pressure gradient.
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PMID:Systemic and portal haemodynamic changes following triglycyllysine vasopressin plus nitroglycerin administration in patients with hepatitis B-related cirrhosis. 211 37


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