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-adrenergic inotropic responsiveness during ischemia
Abteilung für Pathophysiologie, Zentrum für Innere Medizin des Universitätsklinikums Essen, 45122 Essen, Germany
We tested
whether or not endogenous nitric oxide (NO) attenuates 
-adrenergic
inotropic responsiveness during normoperfusion or moderate myocardial
ischemia. In 13 anesthetized pigs with a cannulated left
anterior descending (LAD) coronary artery, the maximal contractile
responses to intracoronary dobutamine and calcium were assessed during
normoperfusion and at the end of a 90-min period of moderate
ischemia (50% reduction in coronary arterial inflow) without
(group 1, n = 6) and with (group
2, n = 7) prior inhibition of NO synthesis [30
mg/kg iv N
-nitro-L-arginine
(L-NNA)]. Contractile function was assessed by a regional
work index (sonomicrometry, micromanometry, mm · mmHg). In
groups 1 and 2 during normoperfusion, the maximal
increase of the work index was greater with calcium than with
dobutamine. At the end of ischemia in group 1, the
baseline work index was decreased by ~50%, and the subsequent
maximal increase of the work index with dobutamine, but not with
calcium, was reduced compared with normoperfusion. In group
2 during normoperfusion, L-NNA did not alter the
maximal increases of the work index with dobutamine or calcium. At the
end of ischemia, the baseline work index was reduced by 64%,
and the subsequent maximal increases of the work index with both
dobutamine and calcium were reduced compared with normoperfusion;
however, the response to calcium was still greater than that to
dobutamine. We conclude that endogenous NO does not limit
-adrenergic inotropic responsiveness in normoperfused or moderately
ischemic porcine myocardium.
nitric oxide; myocardial function; ischemia; dobutamine; calcium
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