Prevention of myocardial injury by pretreatment with verapamil hydrochloride prior to experimental brain death: efficacy in a baboon model.
Systemic and pulmonary hemodynamics were studied in two groups of Chacma baboons following the induction of brain death. Group A was a control group of 11 animals who underwent brain death. They showed significant increments of mean systemic arterial, left atrial, and pulmonary arterial pressures; of systemic vascular resistance, heart rate, and pulmonary artery blood flow; and a reduction in aortic blood flow during the induction of brain death. As a result of increased sympathetic nervous system activity, areas of myocardial cell necrosis occurred in 73% of the animals and pulmonary edema in 36%. Group B consisted of five animals that were pretreated with verapamil hydrochloride infused over a period of 30 minutes prior to the induction of brain death (mean dosage, 0.26 mg/kg). Except for a rise in heart rate, no significant changes occurred in systemic or pulmonary hemodynamics, and no myocardial or pulmonary histopathological changes were seen. These findings would indicate that verapamil hydrochloride prevents both the peripheral and central hemodynamic changes that result from increased sympathetic activity associated with the induction of brain death, and thus prevents myocardial structural damage, which may be associated with increased calcium uptake by the myocyte.
D000818:Animals; D001926:Brain Death; D006321:Heart / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D010215:Papio; D011652:Pulmonary Circulation / Q000187:drug effects; D014019:Tissue Donors; D014700:Verapamil / Q000627:therapeutic use*
D014700:Verapamil