Reperfusion at reduced flow rates enhances postischemic contractile
recovery of perfused heart.
Takeo, Satoshi, Jian-Xun Liu, Kouichi Tanonaka, Yoshihisa Nasa, Kenichi Yabe,
Hiroaki Tanahashi, and Hirokazu Sudo.
Department of Pharmacology, Tokyo University of Pharmacy and Life Science,
Hachioji 192-03, Japan
APStracts 2:0011H, 1995.
The effects of reperfusion at reduced flow rates on postischemic cardiac
contractile function were examined in perfused rat hearts. Isolated hearts
were subjected to 35-min ischemia followed by reperfusion at the preischemic
flow rate (9.0 ml/g/min; ordinary-flow rate) or at reduced flow rates ranging
from 0.9 to 8.1 ml/g/min. Reperfusion at the ordinary-flow rate did not
generate any left ventricular developed pressure (LVDP), whereas reperfusion
at reduced flow rates ranging from 0.9 to 7.2 ml/g/min elicited 13 to 57% of
initial contractile force at the end of reperfusion; the optimal recovery was
achieved at a flow rate of 3.6 ml/g/min (reduced-flow rate). Reperfusion at
reduced-flow rate attenuated ischemia/reperfusion-induced increase in left
ventricular end-diastolic pressure (LVEDP) and perfusion pressure, alteration
in tissue sodium, potassium, calcium and magnesium ions, release of creatine
kinase and ATP metabolites, and the development of triphenyltetrazolium
chloride-unstained areas. Enhanced postischemic LVDP recovery was inversely
related to higher perfusion pressure of the heart at the initial stage (4
min) of reperfusion (r=-0.763). The benefit of reperfusion at a reduced-flow
rate could not be attributed to either the rate of calcium delivery to the
heart, formation of oxygen free radicals of the myocardium, endothelium
-dependent coronary artery dilation or reduction of LVEDP. The enhancement of
postischemic LVDP recovery was associated with an attenuation of
ischemia/reperfusion-induced increases in myocardial sodium and calcium
contents, and the failure of postischemic LVDP recovery was accompanied by an
increase in these contents. A reduction in sodium and calcium overload may
underlie the beneficial effects of reperfusion at reduced-flow in the
ischemic/reperfused heart.
Received 19 January 1994; accepted in final form 10 January 1995.
APS Manuscript Number H52-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 February 1995.