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The Journal of Thoracic and Cardiovascular Surgery, Vol 104, 1365-1374, Copyright © 1992 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
PR Evora, PJ Pearson and HV Schaff
Canine hearts were arrested with crystalloid cardioplegic solution (45
minutes at 7 degrees C) to determine whether either cardioplegia or
hypothermia impairs the production of endothelium-derived relaxing factor
or damages the vascular smooth muscle of epicardial coronary arteries. In
addition, isolated coronary artery segments were exposed to either cold (7
degrees C) or warm (37 degrees C) crystalloid cardioplegic solution and
physiologic salt solution in vitro for 45 minutes. After cardiac arrest or
incubation with the solutions, segments of epicardial coronary artery were
prepared and studied in organ chambers. Cardioplegic arrest of the heart or
exposure to cardioplegic solution in vitro (7 degrees or 37 degrees C) did
not alter endothelium-dependent relaxation of epicardial coronary artery
segments in response to adenosine diphosphate or acetylcholine (10(-9) to
10(-4) mol/L). Cardioplegic arrest did not alter G protein-mediated,
endothelium-dependent relaxation in response to sodium fluoride. In
addition, smooth muscle contraction in response to potassium ions
(voltage-dependent) or prostaglandin F2 alpha (receptor-dependent) and
relaxation in response to isoproterenol (cyclic adenosine monophosphate-
mediated) or sodium nitroprusside (cyclic guanosine monophosphate-
mediated) was unaltered after exposure to cardioplegic solution or
hypothermia. These experiments demonstrate that hyperkalemic crystalloid
cardioplegia does not irreversibly alter function of epicardial coronary
arteries. We hypothesize that coronary artery endothelial cell dysfunction
identified in previous studies of cardioplegia may have been due to the
effects of barotrauma or shear stress on the vasculature and not the effect
of cardioplegia per se.
ARTICLES
Crystalloid cardioplegia and hypothermia do not impair endothelium- dependent relaxation or damage vascular smooth muscle of epicardial coronary arteries
Section of Cardiovascular Surgery, Mayo Clinic, Rochester, MN 55905.
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