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)

One hundred and eight patients with cirrhosis (23 grade A, 46 grade B and 39 grade C, according to Pugh's classification) underwent hemodynamic studies and plasma catecholamine concentration measurements. Blood samples were withdrawn from the pulmonary artery (n = 108), the hepatic vein (n = 108), the azygos vein (n = 59), the right renal vein (n = 66), the right jugular vein (n = 34) and the femoral vein (n = 33). Plasma noradrenaline concentrations in the pulmonary artery and the hepatic vein were more elevated in grade B (607 +/- 52 and 402 +/- 42 pg/ml, respectively) and C patients (630 +/- 59 and 475 +/- 53 pg/ml, respectively) than in grade A patients (411 +/- 51 and 243 +/- 40 pg/ml, respectively). Plasma noradrenaline concentrations from these two vessels were negatively correlated with indocyanine green clearance. These results indicate that both overall and splanchnic sympathetic activities are dependent on altered hepatic function. Significant correlations were found between the wedged hepatic venous pressure and plasma noradrenaline concentrations from either the pulmonary artery, the hepatic vein or the azygos vein. These correlations indicate that both overall and splanchnic sympathetic activities are dependent on the degree of portal hypertension. Moreover, significant correlations were found between hepatic venous plasma noradrenaline concentrations and systemic hemodynamic values, suggesting that splanchnic sympathetic nervous activity could either play a role in the systemic hyperkinetic syndrome or be a consequence of this hyperkinetic syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional sympathetic activity, severity of liver disease and hemodynamics in patients with cirrhosis. 174 20

During a hemodynamic study, plasma catecholamine concentrations were measured in the pulmonary artery and in the hepatic vein in 18 presinusoidal portal hypertensive patients. Results were compared with those in 15 nonportal hypertensive subjects and in 24 cirrhotic patients in good condition (grade A, according to Pugh's classification). Plasma norepinephrine concentrations in the pulmonary artery or in the hepatic vein were not significantly different between nonportal hypertensive subjects (mean +/- S.E.M.: 271 +/- 36 and 83 +/- 11 pg/ml, respectively) and presinusoidal portal hypertensive patients (273 +/- 33 and 84 +/- 11 pg/ml, respectively). These concentrations were, however, elevated in cirrhotic patients (408 +/- 47 and 256 +/- 45 pg/ml, p less than 0.05 in comparison with the two other groups). These differences suggest that increased sympathetic nervous activity in cirrhosis is associated with the presence of liver disease or increase in sinusoidal pressure. Differences in plasma epinephrine concentrations were not significant among the three groups of patients. However, the existence of a significant correlation between pulmonary artery plasma epinephrine concentration and cardiac index (r2 = 0.46, p less than 0.01) in patients with presinusoidal portal hypertension suggests that the adrenal medulla could play a role in the pathophysiology of the hyperkinetic syndrome of these patients.
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PMID:Plasma catecholamines in patients with presinusoidal portal hypertension: comparison with cirrhotic patients and nonportal hypertensive subjects. 202 95

Dopamine may be used in cirrhotic patients with renal or circulatory failure, but this drug can also increase the degree of portal hypertension. Hence, the systemic and splanchnic hemodynamic effects of dopamine have been studied in portal hypertensive rats with secondary biliary cirrhosis. The dose-response curves showed that dopamine significantly increased portal pressure at the same dose (80 micrograms min-1 kg-1 body wt.) in normal and biliary cirrhotic rats. Arterial pressure only increased with higher doses of dopamine in rats with biliary cirrhosis (160 micrograms min-1 kg-1 body wt.) while in normal animals it increased (80 micrograms min-1 kg-1 body wt.). Dopamine (160 micrograms min-1 kg-1 body wt.) significantly increased mean arterial pressure in normal and biliary cirrhotic rats. It significantly increased cardiac output in biliary cirrhotic rats from 134 +/- 6 to 153 +/- 7 ml/min but not in normals. Accordingly, systemic vascular resistance increased significantly in normal rats but not in cirrhotics. Portal pressure increased significantly in normal rats from 8.0 +/- 0.3 to 12.1 +/- 0.6 mmHg and in rats with biliary cirrhosis from 15.9 +/- 1.0 to 19.0 +/- 1.3 mmHg. Portal tributary blood flow increased significantly in normal and biliary cirrhotic rats (14.1 +/- 1 to 20.9 +/- 2.3 ml/min and 18.0 +/- 0.9 to 25.5 +/- 1.8 ml/min, respectively). This study shows that an elevated dose of dopamine increases the hyperkinetic syndrome in rats with secondary biliary cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of dopamine in conscious rats with secondary biliary cirrhosis. 225 34

It has been demonstrated that serotonin (5-hydroxytryptamine; 5HT) can decrease portal vascular resistance in animals and could be a possible mediator for intestinal vasodilatation. Moreover, isolated mesenteric vein from portal hypertensive rats has been shown to be hyper-responsive to 5HT. Hence 5HT may play a role in the pathophysiology of the hyperkinetic syndrome observed in patients with portal hypertension. This hypothesis that serotonin might increase splanchnic blood flow, and hence portal pressure, led us to propose that 5HT receptor antagonists might decrease portal hypertension. We observed that acute administration of ketanserin, an antagonist of serotonin at 5HT2 receptors, significantly decreased portal pressure and portal-systemic collateral blood flow in patients with cirrhosis, whereas hepatic blood flow was not modified. Arterial pressure slightly decreased, while cardiac output was not affected by ketanserin. These findings were also observed during continuous administration of ketanserin. More recently, it has been shown that ritanserin, a more specific 5HT2 receptor antagonist, significantly decreased portal pressure in cirrhotic patients. Finally, in rats with portal hypertension, ketanserin as well as ritanserin produced significant reductions in portal pressure but did not modify portal tributory blood flow. In these portal hypertensive animals, 5HT2 antagonists may act on hepatocollateral vascular resistance. These studies confirm current evidence in favor of a role for the actions of serotonin via 5HT2 receptors in portal hypertension and add a new group of substances for its treatment.
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PMID:Portal hypertension: serotonin and pathogenesis. 228 48

Hyperkinetic circulatory state is common in patients with cirrhosis but the cause of this syndrome has not been clearly elucidated. Systemic hemodynamic changes and their relationship to liver failure and splanchnic hemodynamics were studied in 100 patients with cirrhosis and were compared to a group of 15 patients without portal hypertension. Cardiac output was significantly higher and systemic vascular resistance was significantly lower in cirrhotic patients than in control patients. Multivariate analysis revealed that among different clinical, biochemical and splanchnic hemodynamic data, serum albumin, serum bilirubin, plasma prothrombin, and gastrointestinal bleeding significantly and independently explained the variation of cardiac output and systemic vascular resistance. No relationship was found between hepatic venous pressures or the presence of ascites and the hyperkinetic syndrome. From these results, it is concluded that in patients with cirrhosis liver failure is partly responsible for the hyperkinetic state.
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PMID:[Systemic circulatory hyperkinetic syndrome in patients with cirrhosis. Relation with hepatocellular failure and portal hypertension]. 673 39

In chronic liver disease, the incidence of cirrhosis is increasing. About 1 million deaths from cirrhosis are reported annually by WHO, occupying the 11th position in the hierarchy of pathologies that cause death (1). The prevalence of cirrhosis is often underestimated based on the fact that one third of the patients are asymptomatic (2). Regardless of whether it is elective or urgent extra-hepatic surgery, operative interventions in this range of patients are burdened by an increased risk of perioperative morbidity and mortality (3,4). This reality requires the evaluation of the benefit-risk balance for each patient with the surgical firm indication. A journal of the medical literature, presented over the period 1995-2018 (PubMed), noted that the most frequent extrahepatic interventions in the cirrhotic patient were addressed to the cholecyst and CBD (23%), parietal defects (hernias, events) in 17 %, gastric pathology (19%) and rectum-colon (19%).v Liver cirrhosis is frequently associated with abnormalities of coagulation mechanisms: thrombopenia and platelet dysfunctions, decreased coagulation factors but also proteins involved in fibrinolysis. Cardio-circulatory changes are all the more important as the cirrhotic pathology is more evolved, being expressed by hyperkinetic syndrome and systemic vasodilation with hyper-flow, tachycardia and low peripheral resistance (5). The "trigger" element of these anomalies is the portal hypertension and the porto-systemic shunts that involve vasodilating mediators but also the compensatory activation of the renin-angiotensin system (6). The perioperative anaesthetic strategy in the patients is integrated in a multidisciplinary effort of specific management.
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PMID:Digestive Surgery at the Cirrhotic Patient. 3311 87