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Biomedical subjects

C Bataille

Publications and source records attributed to C Bataille.

At least 19 recordsLinked to original sources
PubMed1985

Acute effects of captopril on systemic and renal hemodynamics and on renal function in cirrhotic patients with ascites.

The reduction of angiotensin II production by captopril--an angiotensin-converting enzyme inhibitor--could suppress hyperaldosteronism without impairment of renal function and could thereby be useful in the treatment of ascites in patients with cirrhosis. Systemic and renal hemodynamics and renal function were studied in 6 nonazotemic patients with cirrhosis and ascites with a low-sodium diet before and after oral administration of 25 mg of captopril. Cardiac output and renal blood flow did not change significantly after administration of captopril, whereas mean arterial pressure significantly decreased. Systemic and renal vascular resistances were significantly reduced. There was a statistically significant reduction of glomerular filtration rate, filtration fraction, and urinary output. Plasma renin activity significantly increased in all patients after administration of captopril. A statistically significant correlation was found between the decrease in mean arterial pressure and the reduction of glomerular filtration, but no relationship was found between basal values of plasma renin activity and the other observed variations. We concluded that captopril mainly induces hypotension due to an increase in renal vasodilatation in ascitic patients with cirrhosis.

Ascites↗
PubMed1984

Oral zinc supplementation improves hepatic encephalopathy. Results of a randomised controlled trial.

22 cirrhotic patients with chronic encephalopathy were given oral zinc supplementation or placebo in a double-blind randomised trial. In the group which received zinc acetate 600 mg a day for 7 days, serum zinc had been restored to normal by day 8. On day 8 hepatic encephalopathy, as assessed by a trailmaking test, was improved in the supplemented group but not in the placebo group. There was also a significant increase in blood urea nitrogen in the supplemented group. Short-term oral zinc supplementation probably improved hepatic encephalopathy by correcting the zinc deficiency that compromises conversion of ammonia to urea. The duration of this improvement requires further investigation.

Acetates↗
PubMed1984

Effects of propranolol on renal blood flow and renal function in patients with cirrhosis.

Systemic and splanchnic hemodynamics, renal blood flow, and renal function were studied in 13 patients with cirrhosis both before and 1 h after oral administration of 40 mg of propranolol (acute administration) and 1 mo after continuous administration of this substance at doses reducing the heart rate by 25% (chronic administration). Cardiac output and the gradient between wedged and free hepatic venous pressures significantly decreased after acute and chronic administration of propranolol; mean arterial pressure did not change significantly and systemic vascular resistance significantly increased. Renal blood flow and renal vascular resistance did not change significantly after acute administration of propranolol and renal function did not change significantly after acute or chronic administration of propranolol. We conclude that propranolol does not alter renal function in patients with cirrhosis who are in good physical condition.

Aldosterone↗
PubMed1984

Discrepancy between wedged hepatic venous pressure and portal venous pressure after acute propranolol administration in patients with alcoholic cirrhosis.

In patients with alcoholic cirrhosis, wedged hepatic venous pressure closely reflects portal venous pressure. This study was carried out to determine if propranolol-induced reductions in portal venous pressure are accurately evaluated by the measurement of wedged hepatic venous pressure. Hepatic venous cannulation and percutaneous transhepatic catheterization of the portal vein were simultaneously performed in 7 patients with alcoholic cirrhosis. One hour after oral administration of 40 mg of propranolol, wedged hepatic and portal venous pressures significantly decreased from 24.3 +/- 3.5 (mean +/- SD) to 19.0 +/- 3.0 mmHg, and from 24.7 +/- 3.9 to 22.4 +/- 3.6 mmHg, respectively. Although no significant difference was found between baseline wedged hepatic and portal venous pressures, a significant difference was found between these pressures after propranolol administration. We concluded that during acute administration of a drug acting on the splanchnic circulation, the measurement of wedged hepatic venous pressure may not provide a reliable estimation of the magnitude of the changes in portal venous pressure. There is, however, no evidence that the direction of the changes might not be adequately assessed by wedged hepatic venous pressure measurement.

Aged↗
PubMed1984

[Systemic circulatory hyperkinetic syndrome in patients with cirrhosis. Relation with hepatocellular failure and portal hypertension].

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.

Adult↗
PubMed1980

[Physiopathology of non-ketotic hyperosmolar coma in diabetes (author's transl)].

Hyperosmolar diabetic coma is characterised by extreme hyperglycaemia and dehydration. Hypernatremia often contributes additionally to plasma hyperosmolarity. The pathogenesis of these component abnormalities is considered. The explanation of the absence of hyperketonaemia is examined in the light of recent experimental and clinical data. At the beginning of the development of the syndrome, high peripheral plasma insulin probably explains the lack of ketosis via inhibition of lipolysis. Later, when hyperosmolar coma is established, peripheral insulinopenia but an "insulinised" liver may coexist. This would favour metabolism of free fatty acids along nonketogenic pathways.

Blood↗
PubMedDate not supplied

Hemodynamic changes in patients with portal venous obstruction.

Splanchnic and systemic hemodynamics were evaluated in five adult patients with portal hypertension due to portal venous obstruction and were compared with those of patients with cirrhosis and those of a control group. In patients with portal venous obstruction, the gradient between wedged and free hepatic venous pressures ranged from 2 to 3 mm Hg, as in the control group, and was significantly lower than in patients with cirrhosis. Hepatic blood flow averaged 0.521 +/- 0.127 liter per min per m2 (mean +/- S.D.) and was significantly lower than that measured in cirrhotic and normal patients. Cardiac index averaged 3.788 +/- 0.629 liters per min per m2; this high value for cardiac index was not significantly different from that measured in cirrhotic patients, but was significantly higher than in patients of the control group. It is suggested that a hyperkinetic circulatory state may result from the development of portal-systemic venous collateral circulation in patients with portal venous obstruction having normal liver and hepatic venous pressures.

Adult↗
PubMedDate not supplied

Assessment of beta-adrenergic blockade with propranolol in patients with cirrhosis.

Fourteen patients with cirrhosis and bleeding esophageal varices were treated with propranolol. The dose of propranolol was determined by decreasing the resting heart rate by 25% 12 hr after an oral dose of propranolol which was given twice a day. Significant decreases in the hepatic venous pressure gradient and cardiac output after 1 month of propranolol administration was observed. To assess beta-adrenergic blockade, the isoproterenol test and plasma propranolol levels were evaluated. Increasing doses of isoproterenol were injected to increase the resting heart rate 25 beats per minute (chronotropic dose 25 or CD25 ). Plasma propranolol concentrations were measured in blood samples drawn 4 hr after the last oral dose. The mean CD25 was 5 +/- 2 micrograms before and 146 +/- 84 micrograms after 1 month of propranolol administration. The plasma propranolol level after 1 month of drug administration was 0.69 +/- 0.47 microM per liter i.e. 2.33 +/- 1.59 micrograms per ml. A significant correlation was found between the CD25 measured after continuous propranolol administration and plasma propranolol level. In conclusion, the efficacy of beta-adrenergic blockade was estimated by the isoproterenol test which correlates with the plasma propranolol level in patients with cirrhosis. This study suggests that the isoproterenol test is useful in assessing beta-adrenergic blockade with propranolol in patients with cirrhosis.

Cardiac Output↗
PubMedDate not supplied

[Bullous skin diseases].

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Diagnosis, Differential↗