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Experimental Research Laboratory, Division of Cardiology, University of Louisville, Louisville, Kentucky 40292
We tested the
hypothesis that late preconditioning (PC) against myocardial infarction
is triggered by the formation of nitric oxide (NO). Conscious rabbits
underwent a 30-min coronary occlusion followed by 3 days of
reperfusion. In group I (control
group, n = 10), rabbits were not
preconditioned, whereas in group II (n = 10), they were preconditioned 24 h earlier with a sequence of six 4-min occlusion/4-min reperfusion
cycles. Myocardial infarct size (tetrazolium staining) was reduced by
50% by PC (28.6 ± 3.2% of the risk region in
group II vs. 56.9 ± 5.9% in
controls, P < 0.05). This reduction
in cell death was associated with improved recovery of myocardial
function [systolic thickening fraction (by sonomicrometry) at 3 days: 2.0 ± 11.0% of baseline in group II vs. 
20.0 ± 2.8% in
group I,
P < 0.05].
Group III rabbits
(n = 11) underwent the same protocol
as group II except that the rabbits
received the NO synthase inhibitor
N
-nitro-L-arginine
(L-NNA, 13 mg/kg) before the PC
ischemia. In these animals, infarct size did not differ significantly
from that observed in control rabbits, indicating that
L-NNA completely blocked the
development of late PC against myocardial infarction. In
group IV
(n = 9), rabbits received
L-NNA as in
group III, but without the six
occlusion-reperfusion cycles, and were subjected to the 30-min
occlusion 24 h later. In this group, infarct size did not differ from
that observed in controls, demonstrating that pretreatment with
L-NNA, in itself, did not affect
the extent of cell death. Taken together, these results indicate that,
in the conscious rabbit, the development of late PC against myocardial infarction is triggered by the generation of NO during the PC ischemia.
It is proposed that NO plays a key role in the delayed myocardial
adaptation to ischemic stress.
L-arginine; nitric oxide synthase; oxygen radicals; nitrogen radicals; myocardial ischemia-reperfusion
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