Effects of verapamil on myocardial tolerance to ischemic arrest: comparison to potassium arrest.
This study evaluates the metabolic and physiologic effects of Verapamil on isolated, perfused rat hearts subjected to 1 hour of global ischemia. Hearts were perfused with a modified Krebs-Henseleit bicarbonate buffer with glucose. During working heart perfusion, mean aortic systolic pressure, heart rate, and aortic and coronary flows were measured. Cardiac output and minute work were calculated. In three groups of eight hearts, 60-minute global ischemia was followed by a 40-minute reperfusion to assess physiologic recovery. Three groups of 11 hearts were assayed for myocardial high-energy phosphates after ischemia. Untreated hearts recovered less than 15% of function and lost 50% of their high-energy phosphate stores. Hearts treated with Verapamil (2 microg/cc) prior to ischemia recovered greater than 85% of function and retained normal adenosine triphosphate (ATP) and 40% decreased creatine phosphate (CP) levels. The metabolic and physiologic effects of Verapamil lasted 20 minutes longer than potassium, possibly related to membrane binding and dissociation of Verapamil. Verapamil was shown to have cardioplegic and protective effects, both probably secondary to inhibition of calcium flux across the sarcolemmal membrane.
Robb-Nicholson
C
C
Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA.
Currie
W D
WD
Wechsler
A S
AS
D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002314:Cardioplegic Solutions; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006324:Heart Arrest, Induced / Q000379:methods*; D023421:Models, Animal; D017202:Myocardial Ischemia / Q000139:chemically induced / Q000503:physiopathology*; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014700:Verapamil / Q000494:pharmacology*
D002121:Calcium Channel Blockers; D002314:Cardioplegic Solutions; D014700:Verapamil; D011188:Potassium