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 effect of a synthetic atrial natriuretic peptide (h-ANP, 25 amino acids, Wy-47.663) on blood pressure, renal electrolyte excretion, plasma catecholamines, and plasma renin activity was studied in nine patients with cirrhosis of the liver and ascites. The peptide was infused intravenously at 24-h intervals for 2 h in groups of four patients each in two different doses (0.015 and 0.075 micrograms/kg/min or 0.06 and 0.3 micrograms/kg/min). A control experiment with the vehicle was performed in all patients. In three patients h-ANP (1 and 2 micrograms/kg i.v.) was administered as an intravenous bolus injection. Consistent falls in blood pressure were observed during h-ANP infusion only with the two higher doses. The two lower infused doses induced a consistent natriuresis; this renal response was abolished when the two larger doses were used. When given as a bolus, h-ANP had a natriuretic effect comparable to that of the two lower doses of infused h-ANP. Plasma catecholamines and plasma renin activity increased during infusion of the two higher doses of h-ANP. It thus appears that in patients with cirrhosis and ascites, the natriuretic effect of infused h-ANP decreases rather than increases when the doses are raised. Bolus administration of h-ANP may be less prone to trigger counterbalancing responses and side-effects.
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PMID:Atrial natriuretic peptide administered as intravenous infusion or bolus injection to patients with liver cirrhosis and ascites. 246 99

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.
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PMID:Natriuretic factors and lithium clearance in patients with the syndrome of inappropriate antidiuretic hormone (SIADH) 250 58

The circadian variations in atrial natriuretic peptide (ANP), plasma renin activity (PRA) and plasma aldosterone (PA) have been investigated in a group of 6 patients with compensated cirrhosis of the liver compared with a group of 6 healthy subjects. All studied subjects were kept for a week on standardized life conditions, with a defined daily intake of 120 mEq of sodium and 60 mEq of potassium. Venous blood samples were collected during a whole day at 6, 8, 12, 18, 20 and 24 hours, with the subjects resting in the clinostatic position during the study. Plasma levels of ANP, PRA and PA were determined by radioimmunoassay. The data were analyzed by the cosinor method. The results show that healthy subjects present a significant circadian rhythm for the three biological variables, while patients with cirrhosis of the liver present a significant rhythm for PA only. Acrophase and amplitude of PA do not present any difference between control and patient groups. The levels of PRA and ANP are significantly higher in the cirrhotic patients. These data suggest in cirrhosis a deep variation in the secreting rhythm of PRA and ANP with maintenance, even at higher levels, of intrinsic PA rhythm. This is a possible index of time-related alterations of water-electrolyte balance and cardiovascular processes in liver cirrhosis.
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PMID:[Circadian rhythm of atrial natriuretic peptide, plasma renin and aldosterone activity in healthy subjects and in patients with compensated liver cirrhosis]. 252 93

Plasma levels of immunoreactive atrial natriuretic peptide (ANP), plasma renin activity (PRA), and plasma aldosterone (PA) were measured for an entire day at 6:00 am, 8:00 am, 12:00 pm, 6:00 pm, 8:00 pm, and 12:00 am in 6 healthy subjects, in 10 patients with compensated cirrhosis of the liver, and in 10 cirrhotics with ascites. The subjects, after synchronized standard life conditions lasting for 6 days were held in a clinostatic position during the study. The data were analyzed by the "cosinor" method. The results show significant circadian rhythms for the three biological variables in healthy subjects. In the compensated cirrhotic group, a circadian rhythm was detected only for PA. No rhythm was demonstrated in the ascitic patients. These data suggest that in cirrhosis of the liver, great variations in secretion rhythmicity for PRA and ANP are present, while maintaining the intrinsic PA rhythmicity, which is lost in patients with ascites. This progressive derangement in PA circadian rhythm in the ANP-PRA-PA system can be considered as an index of evolution in the natural history of cirrhosis of the liver.
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PMID:Atrial natriuretic peptide-renin-aldosterone system in cirrhosis of the liver: circadian study. 252 47

The natriuretic effect of pharmacological doses of atrial natriuretic peptide (ANP) is markedly reduced in cirrhosis with ascites. The current study, which includes two protocols, was carried out to investigate whether this phenomenon is related to the altered systemic hemodynamics present in cirrhosis. In protocol A, the administration of ANP (2.5 micrograms.kg-1 as a bolus followed by a constant infusion of 0.1 microgram.kg-1.min-1) to 10 rats with carbon tetrachloride-induced cirrhosis and ascites produced a significantly lower increase in diuresis (13.4 +/- 1.3 microliters/min) and natriuresis (2.3 +/- 0.3 mu Equiv/min) than in 10 control rats (56.3 +/- 1.4 microliters/min and 8.7 +/- 0.5 mu Equiv/min, respectively), indicating a renal resistance to the effect of ANP in this experimental model of cirrhosis. The reduction of arterial pressure induced by ANP was similar in both groups. However, since baseline mean arterial pressure was significantly lower in cirrhotic rats, the degree of hypotension during ANP infusion was also greater in this group of animals (82 +/- 3 vs. 109 +/- 2 mmHg). The aim of protocol B was to assess whether normalization of arterial pressure in cirrhotic rats increases the renal response to ANP. This protocol includes two groups of 10 rats with cirrhosis and ascites infused with a glucose solution containing norepinephrine (CT-NE rats) or angiotensin II (CT-AII rats) at doses to normalize arterial pressure and an additional control group of 10 cirrhotic rats with ascites receiving only glucose solution (CT rats). Angiotensin II, but not norepinephrine or glucose solution administration, was associated with a significant increase in urine volume and sodium excretion. During ANP infusion, CT rats showed a blunted diuretic and natriuretic response. In contrast, the ANP-induced increase in urine volume and sodium excretion observed in CT-NE (53.6 +/- 10.4 microliters/min and 9.3 +/- 2.2 mu Equiv/min) and CT-AII rats (98.3 +/- 11.6 microliters/min and 15.5 +/- 2.9 mu Equiv/m), was similar or even greater than that showed by the healthy rats of protocol A. The degree of hypotension during ANP administration was also similar (CT-NE, 104 +/- 2; CT-AII, 108 +/- 5 mmHg). These results suggest that the blunted response to pharmacological doses of ANP in cirrhosis with ascites is related to altered systemic hemodynamics of cirrhosis, which further deteriorates during the infusion of the peptide.
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PMID:Role of altered systemic hemodynamics in the blunted renal response to atrial natriuretic peptide in rats with cirrhosis and ascites. 253 Feb 68

The plasma levels of atrial natriuretic peptide (ANP) have been determined by direct radioimmunoassay in 36 clinically-healthy subjects, 24 patients with compensated cirrhosis of the liver, and 20 patients with cirrhosis and ascites. When compared with controls, plasma levels of ANP in compensated cirrhosis do not demonstrate a significant difference (p greater than 0.05). Patients with decompensated cirrhosis of the liver show significantly (p less than 0.001) higher levels of ANP with respect to the controls and to compensated patients. In the control group, a significant (p less than 0.001) negative correlation between plasma levels of ANP and plasma renin activity and plasma aldosterone is demonstrated. The patients without ascites do not present any correlation between these variables (p greater than 0.05). The patients with ascites show a significant (p less than 0.01) positive correlation between ANP and plasma renin activity and plasma aldosterone levels. These results and other data suggest that ANP, although appearing to have plasma levels correlated with the disease stage, and with increases in both renin activity and plasma aldosterone levels, does not seem to have a very important role in sodium retention, or in genesis of ascites in cirrhosis of the liver. Activation of the renin-angiotensin-aldosterone system, activation of the sympathetic nervous system, and the circulatory modifications as well as other mechanisms seem to be more important in the formation of ascites in cirrhotic patients.
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PMID:Plasma levels of atrial natriuretic peptide in compensated and decompensated cirrhosis of the liver. Relationship with the renin-aldosterone system. 253 27

Plasma levels of human atrial natriuretic peptide (hANP) were investigated in patients with liver cirrhosis, and the relationships between plasma hANP levels and the following factors were studied: presence of ascites, serum and urine electrolytes, plasma renin activity, angiotensin I and II, aldosterone, catecholamines, prostaglandin derivatives, conventional liver function tests and circulating blood volume. Plasma hANP level was significantly (P less than 0.05) elevated in patients with ascites (mean = 58.6 pg/mL, s.e.m. = 8.8) compared with cases without ascites (mean = 36.6 pg/mL, s.e.m. = 2.6). With the disappearance of ascites, the level fell to normal in most cases. Urine sodium excretion was positively correlated with plasma hANP in patients without ascites, but not in patients with ascites. The plasma hANP level was disproportionately high for the rate of urinary Na excretion in cirrhotics with ascites. The plasma hANP level was not correlated with any of the other factors such as blood volume, renin-angiotensin-aldosterone levels, catecholamines and liver function tests. These results suggest that plasma hANP levels are elevated in cirrhotic patients especially with ascites, but the natriuretic response of the kidney to this raised hANP level can be impaired in patients with liver cirrhosis and ascites.
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PMID:Plasma human atrial natriuretic peptide levels in patients with liver cirrhosis. 253 28

The present study aimed to assess relationships between plasma levels of atrial natriuretic peptide (ANP) and plasma volume, systemic vascular resistances, cardiac output and plasma renin activity in patients with cirrhosis. Thirty patients were included: eight with no history of liver disease were used as controls; 22 patients had biopsy-proven alcoholic cirrhosis without ascites (n = 11) and with ascites (n = 11). Mean ANP plasma level was significantly higher in both groups of cirrhotic patients than in controls (P less than 0.05). In the control group, ANP and plasma renin activity were inversely correlated (P less than 0.05) but no correlation was found in cirrhotic patients. In the group of patients with ascites, ANP plasma levels were inversely correlated to plasma volume (P less than 0.05) and to cardiac output (P less than 0.01) and directly correlated to systemic vascular resistances (P less than 0.01). Using multiple regression analysis, ANP remained correlated only with systemic vascular resistances (P less than 0.05). These results suggest that cirrhotic patients have high plasma levels of ANP whether or not they have ascites. In the light of current knowledge of ANP actions, the relationships between ANP plasma levels and plasma volume, cardiac output, and systemic vascular resistances are paradoxical in cirrhotic patients with ascites. ANP does not seem to play a critical role in the pathogenesis of sodium and water retention observed in these patients.
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PMID:Atrial natriuretic peptide, plasma renin activity, plasma volume, systemic vascular resistance and cardiac output in patients with cirrhosis. 253 41

Cirrhosis is associated with several circulatory abnormalities. A hyperkinetic circulation characterized by increased cardiac output and decreased arterial pressure and peripheral resistance is typical. Despite this hyperkinetic circulation, some patients with alcoholic cirrhosis have subclinical cardiomyopathy with evidence of abnormal ventricular function unmasked by physiologic or pharmacologic stress. Florid congestive alcoholic cardiomyopathy develops in a small percentage, but the concurrent presence of cirrhosis seems to retard the occurrence of overt heart failure. Even nonalcoholic cirrhosis may be associated with latent cardiomyopathy, although overt heart failure is not observed. Tense ascites is associated with some cardiac compromise, and removing or mobilizing ascitic fluid by paracentesis or peritoneovenous shunting results in short-term increases in cardiac output. Cirrhosis also appears to be associated with a decreased risk of major coronary atherosclerosis and an increased risk of bacterial endocarditis. Small hemodynamically insignificant pericardial effusions may be seen in ascitic patients. The release of atrial natriuretic peptide appears to be unimpaired in cirrhosis, although the kidney may be hyporesponsive to its natriuretic effects.
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PMID:Cardiac abnormalities in liver cirrhosis. 269 Apr 63

Plasma immunoreactive alpha-human atrial natriuretic peptide (ANP) was measured in six cirrhotic patients with massive refractory ascites, under strict metabolic conditions, while they were receiving a 20-meq sodium diet, both before and at two-hour intervals for eight hours following peritoneovenous shunting (PVS). The mean preoperative level of ANP was 75 +/- 18 pg/ml, which was found to be significantly higher than the normal range for this laboratory (8 to 24 pg/ml) (p less than 0.05). This value was also significantly higher than the value of 21 +/- 5 pg/ml (p less than 0.05) obtained in six patients with cirrhosis but without ascites. Following shunt insertion, an immediate natriuresis and diuresis were observed in five of the six cirrhotic patients with refractory ascites. In these five, right atrial pressure and ANP rose immediately, followed by a rise in the level of urinary cyclic guanosine monophosphate. The sixth subject had a delayed rise in right atrial pressure, and correspondingly the rise in ANP, the diuresis, and natriuresis were delayed. The changes in ANP following PVS were positively correlated with changes in right atrial pressure (p less than 0.05), urinary cyclic guanosine monophosphate (p less than 0.05), urinary sodium excretion (p less than 0.05), and urine volume (p less than 0.01). These results suggest that ANP may be important in mediating the acute response to PVS.
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PMID:Acute effects of peritoneovenous shunting on plasma atrial natriuretic peptide in cirrhotic patients with massive refractory ascites. 282 65


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