Circulation, Vol 89, 1237-1246, Copyright © 1994 by American Heart Association
M Kitakaze, M Hori, T Morioka, T Minamino, S Takashima, H Sato, Y Shinozaki, M Chujo, H Mori and M Inoue
BACKGROUND: We have previously reported that ischemic preconditioning
increases 5'-nucleotidase activity and adenosine release during ischemia
and reperfusion. However, its direct cause-and-effect relation has not been
proven. To test the idea that the infarct size-limiting effect of ischemic
preconditioning is blunted by inhibition of ectosolic 5'-nucleotidase
activity, we assessed 5'-nucleotidase activity, adenosine release, and
infarct size caused by sustained ischemia with and without an exposure to
alpha,beta,-methylene adenosine 5'-diphosphate (AOPCP) in the
ischemia-preconditioned myocardium. METHODS AND RESULTS: In 67 open-chest
dogs, the left anterior descending coronary artery was cannulated and
perfused with an extracorporeal bypass tube from the carotid artery. After
hemodynamic stabilization, the coronary artery was occluded four times for
5 minutes separated by 5 minutes of reperfusion (ischemic preconditioning,
n = 10). After this procedure, the coronary artery was occluded for 90
minutes followed by 6 hours of reperfusion. Infarct size normalized by the
risk area was smaller than the control group (n = 8, 41.0 +/- 2.6% versus
6.8 +/- 1.9%), although there were no significant differences in the
endomyocardial collateral flow measured at 80 minutes of ischemia (8.5 +/-
1.1 versus 9.4 +/- 1.0 mL/100 g per minute). Ectosolic and cytosolic
5'-nucleotidase activity and adenosine release were increased during
reperfusion in the ischemic preconditioning group compared with the control
group, and the activity of ectosolic 5'-nucleotidase was markedly reduced
by AOPCP (n = 10). AOPCP affected neither adenosine-induced coronary
vasodilation nor increases in myocardial oxygen consumption during an
intracoronary infusion of isoproterenol (n = 10). To test whether the
increase in 5'- nucleotidase activity decreases infarct size, we infused
AOPCP 10 minutes before the ischemic preconditioning procedure and
continued for 60 minutes after the onset of reperfusion (n = 8). AOPCP
blunted the infarct size-limiting effect (infarct size, 38.8 +/- 4.9%).
AOPCP without ischemic preconditioning did not increase infarct size (n =
9). Furthermore, when AOPCP was infused during the ischemic preconditioning
procedure (n = 6) or during 60 minutes of reperfusion (n = 6), the infarct
size-limiting effect was partially blunted (infarct size, 21.3 +/- 2.5% and
19.5 +/- 2.4%, respectively). CONCLUSIONS: Increases in ectosolic
5'-nucleotidase activity and adenosine release are primarily responsible
for the infarct size-limiting effect of ischemic preconditioning. Exposures
to adenosine during the ischemic preconditioning procedure and enhanced
release of adenosine during reperfusion synergistically contribute to the
infarct size-limiting effects.
ARTICLES
Infarct size-limiting effect of ischemic preconditioning is blunted by inhibition of 5'-nucleotidase activity and attenuation of adenosine release
First Department of Medicine, Osaka University School of Medicine, Japan.
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