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1 Cardiovascular Research Institute and Department of Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103; Hackensack University Medical Center, Hackensack, New Jersey 07601; and 2 Department of Physiology, New York Medical College, Valhalla, New York 10595
The goal of
the current study was to determine the effects of cAMP-mediated
coronary reactivity in conscious pigs with stunned myocardium induced
by 1.5 h coronary stenosis (CS) and 12 h coronary artery
reperfusion (CAR). Domestic swine (n = 5) were
chronically instrumented with a coronary artery blood flow (CBF) probe,
hydraulic occluder, left ventricular pressure gauge, wall-thickening
crystals in the ischemic and nonischemic zones, and a coronary sinus
catheter. The hydraulic occluder was inflated to induce a CS with a
stable 38 ± 1% reduction in CBF for 1.5 h. Before flow
reduction and during CAR, cAMP-induced coronary vasodilation was
investigated by forskolin (20 nmol · kg
1 · min1).
Enhanced CBF responses [+62 ± 9%, P < 0.05, compared with pre-CS (+37 ± 3%)] were observed for forskolin at
12 h after CAR as well as for bradykinin and reactive hyperemia.
With the use of a similar protocol during systemic nitric oxide
(NO) synthase inhibition with
N
-nitro-L-arginine (30 mg · kg1 · day1 for 3 days), the enhanced CBF responses to forskolin, bradykinin, and
reactive hyperemia were not observed after CS. Isolated microvessel preparations from pigs (n = 8) also demonstrated
enhanced NO production to direct stimulation of adenylyl cyclase with
forskolin (+71 ± 12%) or NKH-477 (+60 ± 10%) and
administration of 8-bromo-cAMP (+74 ± 13%), which were abolished
by protein kinase A or NO synthase inhibition. These data indicate that
cAMP stimulation elicits direct coronary vasodilation and that this
action is amplified in the presence of sustained myocardial stunning
after recovery from CS. This enhanced cAMP coronary vasodilation is
mediated by an NO mechanism that may be involved in myocardial
protection from ischemic injury.
coronary reactivity; forskolin; ischemia; coronary stenosis; microvessels; coronary blood flow
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