Effects of diltiazem on anoxic injury in the isolated rat heart.
The effect of diltiazem, a calcium channel blocking agent, on anoxic injury was studied in isolated perfused rat hearts. Anoxia for 60 minutes caused a considerable release of creatine kinase and significant cell injury. Reoxygenation of these anoxic hearts for 20 minutes accelerated the creatine kinase release and caused severe cell injury. Reoxygenation of anoxic hearts with diltiazem at a rate of either 2 or 4.5 mg/liter did not reduce creatine kinase release significantly (probability [p] greater than 0.05). However, the higher dosage of diltiazem (4.5 mg/liter during both anoxic and reoxygenation phases resulted in significant (p less than or equal to 0.05) preservation of healthy tissue. The data suggest that diltiazem in the higher concentration prevents cell injury and reduces mitochondrial damage in anoxic injury.
D000332:Aerobiosis; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology*; D003402:Creatine Kinase / Q000378:metabolism; D004110:Diltiazem / Q000494:pharmacology* / Q000627:therapeutic use; D004305:Dose-Response Relationship, Drug; D006321:Heart / Q000187:drug effects; D000860:Hypoxia / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D008297:Male; D008929:Mitochondria, Heart / Q000648:ultrastructure; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure*; D010101:Oxygen Consumption; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains
D001552:Benzazepines; D003402:Creatine Kinase; D004110:Diltiazem