Protection of ischemic myocardium by inhibition of contracture in
isolated rat heart.
Tani, Masato, Hiroshi Hasegawa, Yukako Suganuma, Ken Shinmura, Yoko
Kayashi, and Yoshiro Nakamura.
Department of Geriatric Medicine, Keio University School of
Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo 160, Japan
APStracts 3:0316H, 1996.
Protection of the ischemic myocardium by pretreatment with a high dose
of 2,3-butanedione monoxime (BDM) is attributed to the enhancement of
glycolytic ATP production rather than to the inhibition of
contracture during mild ischemia. Our objective was to investigate
whether the inhibition of contracture would protect the arrested
heart during prolonged ischemia. Isolated perfused rat hearts were
subjected to 30 min of low-flow ischemia followed by reperfusion.
Ischemic hearts were treated with BDM (5 mmol/L) after beating
stopped. BDM ameliorated the increase in intraventricular pressure
after ischemia without significant changes in ATP levels and with a
decreased accumulation of lactate. BDM treatment accelerated the
recovery of function and high energy phosphates with reduced
myocardial Ca2+ overload. The results of this study suggested that
inhibition of contracture can protect the heart from ischemia
-reperfusion injury.
Received 14 May 1996; accepted in final form 17 June 1996.
APS Manuscript Number H435-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 August 1996