Drugs online research references
Naunyn Schmiedebergs Arch Pharmacol. 1988 Jul;338(1):88-95.
Antagonistic effects of alpha-adrenoceptor blocking agents on arrhythmias, enzyme release, and myocardial necrosis in isolated rat hearts with coronary occlusion and reperfusion.
Bernauer W, Ernenputsch I.
Department of Pharmacology, University of Freiburg, Federal Republic of Germany.
In isolated perfused rat hearts reperfusion of the occluded left coronary artery led to arrhythmias, their severity depending on the duration of the foregoing period of myocardial ischaemia. Simultaneously, high activities of the myocardial enzyme creatine kinase (CK) were released into the perfusion fluid. Corynanthine, blocking mainly alpha 1-adrenoceptors, and rauwolscine, blocking mainly alpha 2-adrenoceptors, concentration-dependently antagonized the reperfusion-induced arrhythmias (3-30 mumol/l). The most severe kind of arrhythmia, i.e., ventricular fibrillation was completely prevented by 30 mumol/l of either drug. Also arrhythmias occurring already during the period of coronary occlusion were antagonized, as tested with corynanthine. The beta 1-adrenoceptor blocking agent metoprolol (1, and 10 mumol/l) had no effect at all against reperfusion arrhythmias, and the mainly alpha 1-adrenoceptor stimulating agent phenylephrine markedly increased the severity of these rhythm disturbances. The release of creatine kinase during the coronary reperfusion was significantly decreased by corynanthine, while the effect of rauwolscine was smaller and non-significant. Phenylephrine markedly increased the enzyme leakage from the myocardium. In all hearts the extent of the ischaemic and necrotic areas was determined. The percentage of the previously ischaemic area found necrotic at the end of the reperfusion, depended on the duration of the coronary occlusion. Corynanthine in a highly significant way decreased the area of myocardial necrosis, an effect obtained to some extent also with rauwolscine. The findings suggest that alpha-adrenoceptor stimulation is involved in the genesis of arrhythmias and myocardial damage associated with myocardial ischaemia and reperfusion. Possible mechanisms of action of corynanthine and rauwolscine are discussed, especially in view of the interrelationship between alpha-adrenoceptors and slow calcium channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2907102&dopt=Abstract
Biochem Pharmacol. 1985 Feb 15;34(4):521-4.
Inhibition of purified lysosomal phospholipase A1 by beta-adrenoceptor blockers.
Pappu AS, Yazaki PJ, Hostetler KY.
Inhibition of rat liver lysosomal phospholipases is one of the main events that leads to accumulation of tissue phospholipids during drug-induced phospholipidosis. Drug inhibition of lysosomal phospholipase A may occur by direct effects of drugs on the enzyme (or substrate) or by drug-induced increases in intralysosomal pH. Although beta-adrenoceptor blockers have not been reported to cause lipid storage, they do inhibit lysosomal phospholipase A. To investigate the structural requirements for drug inhibition, we studied the effects of six beta-adrenoceptor blockers on purified rat liver lysosomal phospholipase A1. The agents studied include: propranolol, timolol, metoprolol, practolol, atenolol and the combined alpha and beta adrenoceptor blocking agent, labetalol. The drugs varied by two logs in their abilities to inhibit phospholipase A1 activity. The relative inhibitory potencies were propranolol greater than labetalol much greater than timolol greater than metoprolol much greater than practolol greater than atenolol. Our studies identify drug hydrophobicity as a key determinant for phospholipase A1 inhibition. A strong negative correlation was noted between the octanol/water partition coefficients and IC50 for phospholipase inhibition (r = -0.91). The ability of propranolol to inhibit phospholipase A1 was identical for the d, l and the d and l stereoisomers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2857566&dopt=Abstract
Zhongguo Yao Li Xue Bao. 1995 Jan;16(1):32-5.
Assay of metoprolol and alpha-hydroxymetoprolol in human urine by reversed-phase liquid chromatography with direct-injection.
Xie HG, Zhou HH.
Department of Pharmacology, Hu-nan Medical University, Changsha, China.
AIM: To develop an HPLC method with direct injection for the simultaneous determination of metoprolol (M) and alpha-hydroxymetoprolol (HM) in human urine. METHODS: Urine (200 microliters) was diluted with eluate and injected into the chromatograph. Samples were separated on an ODS column by isocratic binary elution and monitored by fluorescence detection. RESULTS: No potential interfering peaks were identified. M and HM gave rapid elution and baseline resolution. The linear curves of both analytes ranged between 0.2 and 100 mg.L-1. The response sensitivity was approximately 0.1 mg.L-1 and the coefficients of variation in the assay were within 8% for both compounds. A typical application in oxidation phenotyping was presented for one healthy volunteer who received 100 mg of oral metoprolol. CONCLUSION: The method can be used for the investigation of genetic polymorphism of metoprolol oxidation in the large populations.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7771192&dopt=Abstract
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