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

The present experiments were designed to evaluate vascular reactivity to angiotensin II in rats with experimental cirrhosis of the liver (induced with CCl4 and phenobarbital) before ascites appearance. The systemic pressor response to angiotensin II in conscious animals and the contractile effect of angiotensin II in isolated femoral arteries were studied. In addition, the effect of high sodium intake on these parameters was also analyzed. Both renin and aldosterone plasma concentrations were similar in control and cirrhotic rats on the normal or on the high sodium diet. Basal mean arterial pressure was higher in control rats than in cirrhotic rats on the normal sodium (116 +/- 4 vs. 101 +/- 4 mmHg (1 mmHg = 133.3 Pa), p less than 0.05) or on the high sodium diet (118 +/- 7 vs. 98 +/- 6 mmHg). No differences in plasma renin activity or plasma aldosterone were found between control and cirrhotic rats. Upon injection of angiotensin II, control rats show a dose-dependent increase in mean arterial pressure which is higher in high sodium than in normal sodium rats. Cirrhotic rats showed a lower hypertensive response to angiotensin II than their corresponding control rats. In addition, no difference between pressor responses to angiotensin II was observed when normal sodium and high sodium cirrhotic rats were compared. On application of angiotensin II, femoral arteries of control and cirrhotic rats exhibited a dose-dependent contraction. However, maximal contraction was higher in high sodium control rats (145 +/- 12 mg) than in normal sodium control rats (99 +/- 6 mg, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary sodium intake on the pressor reactivity to angiotensin II in rats with experimental cirrhosis of the liver. 269 60

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.
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PMID:Pathophysiology of vasopressin in edematous disorders. 269 4

The interrelationship between renal hemodynamics and the renin-angiotensin-aldosterone system in 28 nonazotemic cirrhotic patients has been studied. Patients were divided into three groups: A) Patients without ascites nor edema; B) Patients with ascites and a relatively high sodium excretion (41.9 +/- 12.9 mmol/day); and C) Patients with ascites and very low sodium excretion (4.8 +/- 0.6 mmol/day). Renin and aldosterone levels significantly increased in group C. A significant correlation was observed between plasma aldosterone concentration and urinary sodium excretion, and between plasma renin activity and aldosterone levels. There were no significant differences in urine flow, glomerular filtration rate, effective renal plasma flow, or renal blood flow between the three groups of patients, in spite of marked differences in renin and aldosterone levels. Renal perfusion was not related to plasma renin activity either in the overall sample of patients or in the individual groups. These results show that factors other than total renal perfusion are involved in renin secretion in cirrhosis.
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PMID:Renal hemodynamics and the renin-angiotensin system in cirrhosis. 270 70

Haematic concentrations of catecholamines were found to be higher in cirrhotic patients with ascites, than cirrhotic patients without ascites and controls. In compensated and decompensated cirrhosis, different forms of sympathetic nervous activity were observed. The high catecholamine values in cirrhotic patients and the activation of the renin angiotensin-aldosterone system suggest the use of beta-blockers to reduce sodium-water retention.
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PMID:[Blood catecholamines in liver cirrhosis]. 286 1

Hepatic and respiratory failure, common complications following liver resection for hepatocellular carcinoma (HCC), especially when it is combined with liver cirrhosis, can be overcome by careful management of the circulatory and respiratory systems. Another common complication is intractable ascites which resists conventional therapy, such as, diuretics and protein replacement. Here we report a case in which intractable ascites was successfully treated with propranolol. The patient, a 48-year-old man who underwent liver resection for HCC combined with cirrhosis, started to suffer from ascites about 1 week after surgery. Upon administration of propranolol (1 mg/kg/day) with furosemide, his body weight decreased 500 g/day, returning to the preoperative value in 2 weeks in parallel with the normalization of the PRA. No side effects were observed during the medication period. Propranolol, a beta-adrenergic antagonist, is thought to suppress renin secretion from the juxtaglomerular apparatus in the kidney by blocking its beta-adrenergic receptor, thus suppressing the entire renin-angiotensin-aldosterone system. We concluded that propranolol is a promising drug for intractable ascites encountered with liver cirrhosis.
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PMID:[Effect of propranolol on intractable ascites following liver resection]. 287 20

The diuretic effect of the supine position was evaluated in six patients with cirrhosis and ascites and six with congestive cardiac failure. All patients received 1 mg bumethanide intravenously and were randomly assigned to either bed rest in the supine position or normal daily activity in the upright position for the next six hours. The diuretic response was similar in patients with heart failure and cirrhosis, and was significantly greater in the supine than in the upright position: mean 1,133 v 626 ml/6 h (p less than 0.01). The natriuresis was similarly greater during recumbency: mean sodium 96 v 45 mmol (mEq)/6 h (p less than 0.01), and the excreted potassium in six hours was similar in both postures. The glomerular filtration rate was 100 and 66 ml/min (p less than 0.01) and the heart rate 76 and 83 beats/min (p less than 0.05) in the supine and upright positions, respectively. Plasma concentrations of noradrenaline, renin, and aldosterone rose significantly during the upright position. The results suggest that the attenuated response to intravenous bumethanide in the upright position and during normal daily activity may be due to the activation of several, homoeostatic mechanisms which may reduce the excretion of water and salt.
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PMID:[Effect of posture on the diuretic treatment of decompensated cirrhosis and heart failure]. 291 77

Atrial natriuretic factor (ANF), a recently sequenced cardiac peptide, has been shown to have potent natriuretic, diuretic, and vasodilating effects in several species. We have developed a radioimmunoassay to measure the levels of immunoreactive ANF in human plasma. Plasma levels of ANF in healthy volunteers on a low sodium diet were 9.8 +/- 1.4 pmol/liter and increased to 21.9 +/- 3.0 on a high sodium diet. The levels of atrial natriuretic factor correlated directly with urinary sodium and inversely with plasma renin activity and plasma aldosterone levels. Patients with marked edema due to congestive heart failure had plasma levels of atrial natriuretic factor five times higher than normal (P less than 0.05), whereas patients with cirrhosis and edema had levels that were not different from normal. These results suggest that atrial natriuretic factor plays an important role in the adaptation to increased sodium intake.
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PMID:Plasma levels of immunoreactive atrial natriuretic factor in healthy subjects and in patients with edema. 293 71

The present study was designed to investigate whether cirrhosis with ascites is associated with altered tissue content of atrial natriuretic factor. Atrial extracts from 14 cirrhotic rats with ascites and increased plasma renin activity (PRA) (14.4 +/- 4.6 ng X ml-1 X h-1) and aldosterone concentration (148.3 +/- 17.3 ng/dl) and from 10 control rats (PRA, 3 +/- 0.5 ng X ml-1 X h-1; aldosterone, 34.7 +/- 3.7 ng/dl) were intravenously injected into anesthetized normovolemic rats. Only one extract was assayed in each bioassay rat. Atrial extracts from control rats increased diuresis and natriuresis 513 +/- 91 and 3,029 +/- 752%, respectively (means +/- SE). In contrast, atrial extracts from cirrhotic rats increased urine volume 199 +/- 49% (P less than 0.001) and sodium excretion 546 +/- 132% (P less than 0.001). These results strongly suggest that atrial content of atrial natriuretic factor is reduced in cirrhotic rats as compared with control animals.
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PMID:Atrial natriuretic factor: reduced cardiac content in cirrhotic rats with ascites. 293 85

The ability of the kidneys to excrete sodium and free water is often impaired in patients with cirrhosis. Sodium retention is a sine qua non for ascites formation. The impairment of water excretion causes hyponatremia and hypo-osmolality. In addition, these patients frequently have functional renal failure caused by intense renal vasoconstriction. The renin-angiotensin-aldosterone system and the sympathetic nervous system, which are activated in most cirrhotic patients with ascites, and a nonosmotic hypersecretion of antidiuretic hormone are important mechanisms of sodium and water retention. Angiotensin II and sympathetic nervous activity may also be involved in the pathogenesis of functional renal failure. The renal production of prostaglandins is increased in cirrhotic patients with ascites as a homeostatic response to antagonize the vascular effect of endogenous vasoconstrictors and the tubular action of antidiuretic hormone. Nonsteroidal anti-inflammatory drugs should, therefore, be administered with caution in these patients because they may induce acute renal failure and water retention. Although sulindac inhibits the renal synthesis of prostaglandins in cirrhotic patients with ascites, it appears to have less effect on renal function than do other nonsteroidal anti-inflammatory drugs administered to these patients.
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PMID:Renal function abnormalities, prostaglandins, and effects of nonsteroidal anti-inflammatory drugs in cirrhosis with ascites. An overview with emphasis on pathogenesis. 294 81

Cirrhotic ascites occurs via both overflow and underfill mechanisms. Intrahepatic hypertension activates a hepatic baroreceptor reflex that enhances renal sodium absorption; plasma volume is expanded. As cirrhosis progresses, the hepatoportal Starling forces become sufficiently disturbed to sequester this "overflow" in the peritoneal cavity, which results in ascites formation. "Underfill" of the vascular system occurs and eventually dominates the clinical picture. Finally, intrahepatic hypertension also activates the renin-angiotensin system, which causes renal vasoconstriction; the increase in renal prostaglandin synthesis maintains renal blood flow. Although cirrhotic ascites is traditionally classified as a transudate, the serum-ascites albumin gradient may be a better indicator of ascites secondary to portal hypertension than other causes. General management of patients with cirrhotic ascites includes severe restriction of dietary sodium intake and bed rest; diuretics are added if spontaneous diuresis does not occur after 3 to 4 days.
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PMID:Cirrhotic ascites. Pathophysiology, diagnosis, and management. 294 63


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