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The Journal of Thoracic and Cardiovascular Surgery, Vol 86, 252-261, Copyright © 1983 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
F Yamamoto, AS Manning, MV Braimbridge and DJ Hearse
The ability of dl-verapamil to enhance myocardial protection when given
before, during, or after myocardial ischemia was assessed with the use of
an isolated working rat heart model of cardiopulmonary bypass and ischemic
cardiac arrest. Under conditions of normothermic ischemic arrest (30
minutes at 37 degrees C), the addition of verapamil enhanced the protective
properties of the St. Thomas' Hospital cardioplegic solution. Optimal
protection was observed with verapamil concentrations of 0.5 mg/L (1.09
mumol/L) of cardioplegic solution. Under these conditions, postischemic
enzyme leakage was reduced by 32.2% and the postischemic recovery of aortic
flow was improved by 18.7%. Despite the additional protection at
normothermia, the drug at several concentrations appeared unable to improve
functional recovery after an extended period of hypothermic arrest (150
minutes at 20 degrees C), although under these conditions its inclusion in
the cardioplegic solution could substantially reduce enzyme leakage. In
other studies, the ability of various doses of verapamil alone as a
substitute for the cardioplegic solution was examined. At the optimal dose
(again 0.5 mg/L), and under normothermic conditions, verapamil alone was a
good protection against ischemic injury, although this protection did not
match that afforded by the St. Thomas' Hospital cardioplegic solution. In
similar studies under hypothermic conditions, the drug failed to afford
tissue protection, perhaps indicating some common modality between
hypothermia and verapamil-induced protection. Pretreatment with verapamil
(0.1 mg/L) prior to ischemia offered moderate additional protection, but
its use during reperfusion failed to enhance overall recovery.
ARTICLES
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