Post-ischemic myocardial function after pre-ischemic application of propranolol or verapamil.
The influence of pre-ischemic treatment with propranolol (0.8 mg/kg bw) or with verapamil (0.1 mg/kg bw) on myocardial O2 consumption and on coronary resistance after cardioplegic arrest (300 minutes at 22 degrees - 24 degrees C) was investigated, using a Langendorff technique in open chest experiments (canine hearts). For myocardial protection histidine buffered Bretschneider solution was used, while for standardization all hearts were postischemically reperfused with a modified Tyrode solution at 35 degrees C. Both drugs were given intravenously in two fractions, 60 and 30 minutes before the onset of cardioplegic perfusion; a third group was not pretreated. Although the verapamil group had the lowest O2 consumption post-ischemically, the most impressive results were found in coronary resistance. Propranolol significantly diminished coronary resistance (p less than 0.05), while verapamil distinctly enhanced it compared to the non treated group. The "membrane labilizing" effect of verapamil combined with calcium-free cardioplegic solution was confirmed by a massive postischemic myocardial sodium uptake.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004285:Dogs; D005260:Female; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D006324:Heart Arrest, Induced; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects*; D011433:Propranolol / Q000008:administration & dosage* / Q000494:pharmacology; D014700:Verapamil / Q000008:administration & dosage* / Q000494:pharmacology
D011433:Propranolol; D014700:Verapamil