Reducing lactate accumulation does not attenuate lethal ischemic
injury in isolated perfused rat hearts.
Vander, Richard S., Heide, John A. Delyani, Robert B. Jennings, Keith
A. Reimer, Charles Steenbergen.
Department of Pathology, Duke Univeristy Medical Center, Durham,
North Carolina 27710,
APStracts 2:0312H, 1995.
The role of lactate accumulation in lethal ischemic myocardial cell
injury was assessed by partially depleting hearts of glycogen prior
to ischemia using glucagon. Isolated adult rat hearts were perfused
with glucose-free Krebs Henseleit buffer containing acetate as
substrate. Following stabilization, treated hearts were perfused
briefly (3 minutes) with buffer containing 2 [mu]g/ml glucagon to
reduce tissue glycogen stores, followed by 10 minutes of perfusion
with control buffer, and 60 or 90 minutes of global ischemia. Before
the onset of ischemia, glucagon-treated hearts contained 40% less
glycogen than untreated hearts but myocardial function and tissue
levels of high energy phosphates, lactate, and glucose-6-phosphate
were similar. Lactate production during ischemia in the glucagon
-treated hearts was 50% less than in untreated hearts. However, there
was no decrease in the amount of creatine kinase release during
reperfusion after either 60 or 90 minutes of ischemia. Thus, although
partial glycogen depletion reduced lactate accumulation during
ischemia, this did not decrease the amount of lethal myocardial cell
injury.
Received 17 March 1995; accepted in final form 22 June 1995.
APS Manuscript Number H261-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.