The Journal of Thoracic and Cardiovascular Surgery, Vol 77, 602-607, Copyright © 1979 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Potassium-induced cardioplegia during normothermic cardiac arrest. Morphologic study of the effect of varying concentrations of potassium on myocardial anoxic injury
F Gharagozloo, BH Bulkley, GM Hutchins, TJ Bixler 2d, HV Schaff, JT Flaherty and TJ Gardner
Most corrective procedures as well as myocardial revascularization require
a period of cardiac arrest, and numerous methods have been proposed to
protect the myocardium during this ischemic episode. Potassium-induced
cardioplegia is one method that appears to be of benefit in this setting.
Since it is recognized that myocardial necrosis may result at very high
doses of potassium, we examined the effect of varying concentrations of
potassium on myocardial anoxic injury. Using an isolated rat heart
preparation, we evaluated anoxic injury occurring with cardioplegic
solutions containing various concentrations of K+, ranging from 15 to 200
mEq. per liter, during a 50 minute normothermic arrest followed by 60
minutes of reperfusion. The transverse histologic sections of the left
ventricular myocardium were analyzed for contraction band injury by
morphometric and qualitative methods. Among the 62 animals studied the
least severe anoxic injury was seen with K+ cardioplegia at concentrations
of 25 and 30 mEq. per liter. At lower and higher concentrations there was
little difference between the hearts exposed to anoxia with or without K+
cardioplegia. Potassium administered in very high doses, i.e., 100 or 200
mEq. of K+ per liter, led to contracture and extensive myocardial cell
injury. This study suggests that potassium-induced cardioplegia is
effective in reducing cell injury due to anoxia, and in this model an
optimal concentration range was 25 to 30 mEq. per liter.
