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Articles in PresS, published online ahead of print February 21, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00834.2001
Submitted on September 24, 2001
Accepted on February 13, 2002
1 Experimental Cardiology, Thoraxcenter, Erasmus University Rotterdam, Rotterdam, Zuid-Holland, Netherlands
* To whom correspondence should be addressed. E-mail: duncker{at}tch.fgg.eur.nl.
Left ventricular (LV) dysfunction caused by myocardial infarction is accompanied by endothelial dysfunction, most notably a loss of nitric oxide (NO) availability. We tested the hypothesis that endothelial dysfunction contributes to impaired tissue perfusion during increased metabolic demands as produced by exercise, and determined the contribution of NO to regulation of regional systemic, pulmonary and coronary vasomotor tone in exercising swine with LV dysfunction produced by a 2-3-week old myocardial infarction (MI). LV dysfunction resulted in blunted systemic and coronary vasodilator responses to ATP, whereas the responses to nitroprusside were maintained. Exercise resulted in blunted systemic and pulmonary vasodilator responses in MI that resembled the vasodilator responses in normal swine (N) following blockade of NO synthase with N
-nitro-L-arginine (NLA, 20 mg/kg iv). However, NLA resulted in similar decreases in systemic (43±3% in N and 49±4% in MI), pulmonary (45±10% in N and 49±5% in MI) and coronary (29±4% in N and 34±2% in MI) vascular conductances in N and MI under resting conditions, while similar effects were also observed during treadmill exercise. Selective inhibition of iNOS with aminoguanidine (20 mg/kg iv) had no effect on vascular tone in MI. These findings indicate that while agonist-induced vasodilation is already blunted early after myocardial infarction, the contribution of endothelial NO synthase derived NO to regulation of vascular tone under basal conditions and during exercise is maintained.
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