Verapamil selectively depressed contractility in ischemic myocardium in 5/5 dogs without altering normal myocardium, whereas propranolol depressed contractile function in both.
Does verapamil selectively depress contractility in ischemic myocardium compared to propranolol in open-chest dogs?
Verapamil selectively depresses contractility in ischemic myocardium without affecting normal myocardium, unlike propranolol which depresses both, suggesting a potential mechanism to reduce myocardial oxygen demand and ischemic injury.
The effects of verapamil (0.02-0.2 mg/kg) on contractility in normal and partially ischemic myocardium were compared with the changes following propranolol (0.01-1.0 mg/kg). Regional contractile function was studied in open-chest dogs with ultrasonic crystals and ischemia was controlled by graded occlusion of a carotid-to-coronary artery shunt. Reduction in shunt perfusion pressure (40-55 mm Hg) resulted in hypokinesia. Verapamil depressed contractility in ischemic myocardium in 5/5 dogs, but did not alter the maximum velocity of shortening (max V) or end-diastolic segment length in normal myocardium. Propranolol in doses sufficient to depress ischemic myocardium also depressed contractile function in normal myocardium. In two dogs without coronary occlusion, verapamil (up to 1.0 mg/kg) increased end-diastolic segment length but did not reduce max V. We conclude that verapamil selectively depresses ischemic myocardium, a finding that may have clinical implication since ischemic injury can be decreased by reducing contractility (and thereby MVO2).
Smith et al. (1976) studied Myocardial ischemia (n=7). Verapamil vs. Propranolol was evaluated on Regional contractile function. Verapamil selectively depressed contractility in ischemic myocardium in 5/5 dogs without altering normal myocardium, whereas propranolol depressed contractile function in both.