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1 Cardiovascular Research Institute and Department of Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark 07103; 2 Hackensack University Medical Center, Hackensack, New Jersey 07601; and 3 Cardiology Division, University Texas-Houston Medical School, Houston, Texas 77030
There is
increasing evidence that nitric oxide (NO) produced by inducible
NO synthase (iNOS) plays a key role in cadioprotection during the
"second window of protection" (SWOP). The goals of this study were
to determine 1) whether a transient ischemic episode [10-min coronary artery occlusion (CAO), followed by full
reperfusion] enhances NOS function in cardiac myocytes, 2)
which specific NOS isoform is responsible for the enhanced NOS function
in myocytes, and 3) to localize iNOS expression during SWOP.
To address these questions, 10 dogs were instrumented to measure aortic
and left ventricular pressures and wall thickness. At 1-2 wk after
recovery, myocardial ischemia was induced regionally by a
10-min left circumflex CAO. After 24-h reperfusion, cardiac myocytes
were isolated from the previously ischemic and
nonischemic regions (n = 6). Myocyte contractile function was assessed using a video motion detector at 1 Hz
(35 ± 2°C). At baseline, myocyte contractile function (% contraction) was similar in the two regions (ischemic 7.8 ± 0.5% vs. nonischemic 7.8 ± 0.2%).
L-Arginine (1 mM) significantly reduced
(P < 0.05) myocyte contraction in the ischemic
(
34 ± 3%, P < 0.05) but not (7 ± 4%)
nonischemic regions; these responses were abolished by
NG-nitro-L-arginine (1 mM), a
nonspecific NOS inhibitor, as well as
2-amino-5,6-dihydro-6-methy-4H-1,3,thiazine (1 mM), a specific iNOS
inhibitor. Immunohistochemistry also revealed enhanced iNOS expression
in the myocardium and in particular the interstitial spaces in the
ischemic zone. These results indicate that a brief ischemic episode upregulates iNOS function in myocytes as well as in the interstitial space between blood vessels and myocytes, strategically where it can regulate both vascular and myocyte function
during the SWOP.
preconditioning; nitric oxide; contraction; second window of protection
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