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The Annals of Thoracic Surgery, Vol 24, 307-314, Copyright © 1977 by The Society of Thoracic Surgeons
RE Clark, TB Ferguson, PN West, RC Shuchleib and PD Henry
This study was based on the concept that intracellular accumulation of
calcium plays a role in mediating ischemic myocardial injury and that
inhibition of entry of calcium into cells may have a salutary effect on the
ischemic heart. Nifedipine, a potent vasodilator and inhibitor of
transmembrane calcium flux, was infused into the aortic root of 6 dogs (5
microgram/kg/hr) during 2 hours of myocardial ischemia while on
cardiopulmonary bypass. Seven control animals received normal saline at the
same flow rate and temperature (20 degrees C). The results showed that none
of the 7 control animals were able to maintain adequate aortic pressure or
cardiac output after 30 to 60 minutes of normothermic reperfusion. All had
marked left ventricular failure and were unresponsive to large doses of
inotropic agents. In contrast, the 6 dogs treated with nifedipine were
weaned from bypass either without difficulty or requiring small doses of
calcium chloride and norepinephrine. Light microscopy demonstrated more
marked ischemic damage in the control group than in the group of
drug-treated dogs. We conclude that the concept of inhibition of
transmembrane calcium flux offers a new and potent method for myocardial
preservation during ischemia.
ARTICLES
Pharmacological preservation of the ischemic heart
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