Drugs online research references
Eur J Clin Pharmacol. 1988;35(5):475-81.
Allopurinol prevents ischaemia-dependent haemorheological changes.
Capecchi PL, Pasini FL, Pasqui AL, Orrico A, Ceccatelli L, Acciavatti A, Galigani C, Pieragalli D, Di Perri T.
Istituto di Patologia Medica, Universita di Siena Le Scotte, Italy.
Pre-treatment with allopurinol is able markedly to attenuate the deterioration in blood viscosity (BV) and whole blood filterability (WBF) that occurs after ischaemia during exercise. It also reduces the exercise-induced increase in serum oxidase activity, although this action is slightly less effective in peripheral obliterative arterial disease (POAD) patients. Conversely, allopurinol is completely ineffective in modifying haemorheological parameters in vitro, and it does not affect superoxide anion generation or enzyme release from neutrophils stimulated in vitro with formyl-methionyl-leucyl-phenylalanine (FMLP). It is suggested that allopurinol may attenuate changes in BV and WBF by affecting xanthine-oxidase-dependent free radical formation in tissues.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2853054&dopt=Abstract
Chin J Physiol. 1992;35(1):9-19.
Drug effects on the ischemia- and reperfusion-induced arrhythmias in the conscious rats.
Huang TF.
Department of Physiology, College of Medicine, National Taiwan University, Taipei, Republic of China.
A simple model of coronary occlusion and reperfusion in conscious rat was used to test the effects of various drugs on the arrhythmias. Blood pressure and ECG were monitored on a Grass polygraph. Intravenous infusion of test agents started before coronary occlusion and continued through the periods of occlusion and reperfusion. The free radical scavengers (allopurinol 12.3 mg/kg, mannitol 33.0 mg/kg, N-2-mercapto-propionyl glycine 8.6 mg/kg and adenosine 10.0 mg/kg), class 1-4 antiarrhythmic drugs (lidocaine 10.2 mg/kg, quinidine 12.3 mg/kg, propranolol 4.9 mg/kg, amiodarone 5.6 mg/kg and verapamil 1.1 mg/kg), aspirin 24.5 mg/kg and benadryl 3.7 mg/kg reduced the incidence of ventricular fibrillation and shortened the duration of arrhythmias during occlusion and reperfusion. Cimetidine 6.9 mg/kg was ineffective to exert the antiarrhythmic action. These results implicate that multiple factors, such as ionic channels (Na, K and Ca), free radicals, arachidonate metabolites and histamine release may play significant roles in genesis of arrhythmias during myocardial ischemia and reperfusion.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1424955&dopt=Abstract
Am J Physiol. 1990 Jul;259(1 Pt 1):G134-9.
An in vitro model of ischemia/reperfusion-induced microvascular injury.
Inauen W, Granger DN, Meininger CJ, Schelling ME, Granger HJ, Kvietys PR.
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130.
The major objective of this study was to develop an in vitro model of ischemia/reperfusion (I/R)-induced microvascular injury. Cultured venular endothelial cells were grown to confluency, labeled with 51Cr, and exposed to different durations of anoxia (0.5, 1, 2, 3, and 4 h). 51Cr release and cell detachment (indexes of cell injury) were determined at different times after reoxygenation (1, 2, 4, 6, 8, and 18 h). Because in vivo studies have implicated neutrophils in I/R injury, in some experiments human neutrophils were added to the endothelial cells upon reoxygenation. Periods of anoxia greater than or equal to 2 h resulted in 70-80% 51Cr release and 80-95% cell detachment upon reoxygenation. Under these conditions (near maximal injury), the addition of neutrophils produced negligible effects. Periods of anoxia less than or equal to 1 h resulted in 30-40% 51Cr release and 50-60% cell detachment. Under these conditions (moderate cell injury), addition of neutrophils enhanced endothelial cell injury. Using a 30-min period of anoxia, we also assessed the effects of superoxide dismutase (SOD; 300 U/ml) and allopurinol (20 microM) on anoxia/reoxygenation (A/R)-induced injury in the presence or absence of neutrophils. In the absence of neutrophils, SOD or allopurinol did not protect against A/R-induced injury. However, in the presence of neutrophils, both SOD and allopurinol attenuated the increases in 51Cr release. The results derived using this in vitro model of I/R injury are largely consistent with published in vivo studies. Thus this in vitro model may provide further insights regarding the mechanisms involved in I/R injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2372057&dopt=Abstract
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