Search PubMed⌕ Search

Biomedical subjects

R Brotelle

Publications and source records attributed to R Brotelle.

9 recordsLinked to original sources
PubMed1989

Differential effects of amiodarone and propranolol on lipid dynamics and enzymatic activities in cardiac sarcolemmal membranes.

The amphiphilic cationic cardioactive drugs (pindolol, propranolol and amiodarone) were tested for their effects on lipid dynamics (measured by fluorescence depolarization) and on enzymatic activities up to 1 mM in purified cardiac sarcolemmal vesicles from adult rat. The vesicles were enriched 12- to 37-fold (with respect to tissue homogenate) in Na+/K+ ATPase, K+-stimulated p-nitrophenylphosphatase, 5'nucleotidase and adenylate cyclase, all of which are believed to be components of sarcolemma. Phospholipids and cholesterol content were enriched 5- and 13-fold respectively. There was very little contamination of the sarcolemmal vesicles by sarcoplasmic reticulum (as judged by Ca2+ ATPase and glucose-6-phosphatase activities) or mitochondria (as judged by cytochrome-c-oxidase activity). Pindolol had no effect on lipid dynamics and enzyme activities except for the isoproterenol-stimulated adenylate cyclase. The latter was also totally inhibited at 1 microM by propranolol which inhibited Mg2+ ATPase and increased fluidity above 20 microM. Amiodarone affected all the enzyme activities (except Na+/K+ ATPase): isoproterenol-stimulated adenylate (IC50 = 30 microM), Mg2+ ATPase (IC50 = 20 microM) and K+-stimulated-p-nitrophenylphosphatase were inhibited; 5'nucleotidase was activated above 2 microM. By contrast with propranolol, amiodarone decreased lipid mobility. The effect was linear with the concentration of the drug above 1 microM.

4-Nitrophenylphosphatase↗
PubMed1987

Prevention by amiodarone of phospholipid depletion in isoproterenol-induced ischemia in rats.

This work was performed to study phospholipid metabolism in isoproterenol-induced ischemic heart and the possible protective effect of amiodarone (Am) and chlorpromazine (CPZ). Heart weight increased 24 h after subcutaneous injection of isoproterenol (40 mg/kg) whereas myocardial phospholipid content and creatine kinase activity decreased without modification of the cholesterol content. The phospholipid content was significantly correlated with creatine kinase activity (P less than 0.001). Phosphatidylcholine, phosphatidylethanolamine and cardiolipin decreased significantly (P less than 0.001) in the isoproterenol group whereas the lysophosphatidylcholine and lysophosphatidylethanolamine content increased. The lysophosphatidylcholine/phosphatidylcholine and lysophosphatidylethanolamine/phosphatidylethanolamine ratios consequently increased to a significant degree (P less than 0.01) suggesting indirectly the activation of phospholipases A in the ischemic myocardium. Free fatty acid content increased, indicating hydrolysis of phosphatidylcholine, phosphatidylethanolamine, lysophosphatidylcholine and lysophosphatidylethanolamine. Intravenous injection of Am (20 mg/kg) or intraperitoneal injection of CPZ (30 mg/kg) prior to isoproterenol injection provided complete protection against phospholipid depletion and against increase of the lysophosphatidylcholine/phosphatidylcholine and lysophosphatidylethanolamine/phosphatidylethanolamine ratios which returned to control values. Neither substance had any effect on the heart weight increase due to an edematous and inflammatory process. The total protection by both substances against phospholipid depletion was not sufficient to prevent the creatine kinase activity decrease. The improved phospholipid degradation in the ischemic myocardium is discussed in relation to the in vitro inhibitory effect of Am or CPZ on phospholipases A activity.

Amiodarone↗
PubMed1985

Phospholipid composition of rat lung after amiodarone treatment.

The total phospholipid, cholesterol and protein content was determined in lung, heart and plasma of rats treated with 50, 100 and 150 mg/kg/day p.o. of amiodarone during two weeks. No modification was observed in the heart. The phospholipid and cholesterol content of lung was not modified at the lowest dose but the former increased by 27% and 70% at 100 and 150 mg/kg/day. Phospholipid pattern indicated that phosphatidylcholine content increased selectively. The phospholipid accumulation was totally reversed two weeks after the end of treatment. The results are discussed as a function of the lipid catabolism in the lung.

Amiodarone↗
PubMed1980

Variability in the preventive action of the B-blockers on genetic hypertension in the rat.

Changes in arterial blood pressure were compared in young male SHR rats untreated or treated orally with a beta-blocker for 5 days out of 7 from the 5th to 9th week of life. Propranolol, acebutolol and practolol, at a daily dose of 50 mg/kg, prevented the occurrence of hypertension, not only during the 4 weeks of treatment, but also during 6,9 and 11 weeks respectively after cessation of treatment. Alprenolol and metoprolol (50 mg/kg/day) and atenolol (100 mg/kg/day) proved to be active only during the period of treatment, whereas oxprenolol (100 mg/kg/day) was totally inactive. Propranolol and acebutolol were, however, inactive under identical conditions with SHR of the same strain but bred in another laboratory. The physiological difference between the two groups of SHR was confirmed by the fact that the resistance of their erythrocytes to osmotic shock was different. This suggests that all the beta-blockers do not necessarily have the same preventive activity with respect to hypertension in the SHR and that two groups of SHR bred in two different places can be physiologically dissimilar even though they originate from the same strain.

Acebutolol↗