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Am J Physiol Heart Circ Physiol 279: H451-H456, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 1, H451-H456, July 2000

RAPID COMMUNICATION
Nitric oxide, an important regulator of perfusion-contraction matching in conscious pigs

Raymond K. Kudej1,2, Song-Jung Kim1, You-Tang Shen3, John B. Jackson1, Amelia B. Kudej1, Gui-Ping Yang1, Sanford P. Bishop1, and Stephen F. Vatner1

1 Henry Hood Research Program, Weis Center for Research, Pennsylvania State University College of Medicine, Danville 17822; Department of Cellular and Molecular Physiology and 2 Department of Comparative Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033; and 3 Merck Research Laboratories, West Point, Pennsylvania 19486

We examined whether nitric oxide (NO) inhibition during moderate reduction in coronary blood flow (CBF) would affect perfusion-contraction matching. Coronary stenosis (CS) was induced in conscious pigs, which resulted in a stable 39 ± 1% reduction in CBF for 1.5 h. Ischemic zone wall thickening (IZWT) decreased by an average of 56 ± 2% during CS from 2.7 ± 0.2 mm. After reperfusion, myocardial stunning was observed, but this recovered without evidence of necrosis. After recovery and subsequent administration of systemic NO synthase inhibition (Nomega -nitro-L-arginine, 25 mg · kg-1 · day-1 × 3 days), CS for 1.5 h reduced CBF similarly but decreased IZWT significantly more, P < 0.05, by 89 ± 5%. Myocardial stunning, i.e., the decrease in IZWT at 12 h post-CS, was more severe (-65 ± 5% vs. -21 ± 3%), P < 0.05. Furthermore, CS during NO synthase inhibition resulted in multifocal subendocardial areas of necrosis in the area at risk. These data suggest that in the intact, conscious pig, NO inhibition prevents perfusion-contraction matching, resulting in intensification of post-ischemic stunning and development of subendocardial necrosis.

myocardium; ischemia; infarction; stunning


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