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The Journal of Thoracic and Cardiovascular Surgery, Vol 106, 317-328, Copyright © 1993 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
NM Cohen, RM Wise, AS Wechsler and RJ Damiano Jr
BACKGROUND: Hyperkalemic depolarized cardiac arrest has been the
cornerstone of myocardial protection during cardiac surgery for more than
30 years. Many of the advances in myocardial protection seek to minimize
the cellular damage and to reduce the ongoing metabolic processes occurring
as a direct consequence of the depolarized state. Ideally, cardiac arrest
at hyperpolarized cellular membrane potentials-- the natural resting state
of the heart--will meet all the requirements of modern cardioplegia,
namely, electromechanical asystole and cardiac relaxation, while preserving
the vital integrity of the heart itself. METHODS AND RESULTS: To determine
whether activation of adenosine triphosphate-sensitive potassium channels
by pharmacologic agents could produce hyperpolarized cardiac arrest, we
tested the ability of aprikalim, a known adenosine triphosphate-sensitive
potassium channel opener, to arrest the intact beating heart. In a
normothermic (37 degrees C) isolated rabbit heart preparation, aprikalim
was found to rapidly shorten the action potential duration and produce
cardiac asystole that was maintained during 20 minutes of "no-flow" global
ischemia without a rise in end-diastolic pressure. Cardiac rhythm and
function were fully restored by reperfusion alone (developed pressure was
100.6% +/- 7.9% of prearrest value after 30 minutes of reperfusion). In
contrast, 20 minutes of unprotected normothermic global ischemia resulted
in a 2.7 +/- 0.55 mmHg rise in end-diastolic pressure and only 58.2% +/-
3.8% recovery of developed pressure after 30 minutes of reperfusion. By way
of comparison, 20 minutes of standard hyperkalemic depolarized normothermic
rest was accompanied by a 1.2 +/- 0.6 mmHg rise in end-diastolic pressure
and only 80.8% +/- 2.6% recovery of developed pressure after 30 minutes of
reperfusion. To directly compare hyperkalemic depolarized cardiac arrest to
hyperpolarized cardiac arrest induced by potassium channel openers and to
better define the characteristics of such hyperpolarized arrest, we studied
a fixed (4 mmHg rise in end-diastolic pressure--contracture) ischemic
injury model. The time to development of the contracture was prolonged by
hyperkalemic arrest (35.8 +/- 1.7 minutes) and significantly more so by
hyperpolarized arrest (47.0 +/- 3.3 minutes) when compared with that of
unprotected hearts (24.0 +/- 1.2 minutes). Moreover, aprikalim resulted in
significantly better postischemic recovery of function (developed pressure
was 69.0% +/- 6.7% of prearrest value after 30 minutes of reperfusion) than
after no cardioplegia (45.4% +/- 7.5%) or standard hyperkalemic
cardioplegia (44.3% +/- 5.7%). CONCLUSIONS: Pharmacologic activation of
adenosine triphosphate-sensitive potassium channels can result in
predictable and sustainable hyperpolarized cardiac arrest that is
reversible by reperfusion. This method of myocardial protection was found
to fully preserve cardiac electromechanical function after a 20-minute
period of global normothermic ischemia. Furthermore, hyperpolarized arrest
induced by potassium channel openers significantly prolonged the period to
the development of contracture and afforded a significantly better
postischemic recovery of function than obtained in either hearts protected
with hyperkalemic depolarized arrest or those not protected by any form of
cardioplegia.
ARTICLES
Elective cardiac arrest with a hyperpolarizing adenosine triphosphate- sensitive potassium channel opener. A novel form of myocardial protection?
Department of Surgery, Medical College of Virginia, Richmond 23298-0645.
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