@entity842 inhibits the positive inotropic response to beta-adrenergic stimulation in XXXX with @entity1002 .

@entity1 @entity6306 @entity452 @entity7293 @entity842 @entity453 @entity1002
BACKGROUND: @entity842 (NO) attenuates the contractile response to beta-adrenergic stimulation in cultured cardiac myocytes in vitro and in myocardium in vivo. We tested the hypothesis that NO synthesized in the heart inhibits the positive inotropic response to beta-adrenergic stimulation in @entity1 with @entity1002 . METHODS AND RESULTS: @entity1 with various degrees of @entity1002 and free from @entity453 were instrumented with an infusion catheter in the left main coronary artery and a high-fidelity micromanometer-tipped catheter in the LV. Measurements included LV pressure, aortic pressure, heart rate, and LV peak +dP/dt. In eight subjects, @entity452 was infused via the left main coronary artery (25 or 50 micrograms/min) before and concurrent with intracoronary infusion of the NO synthase inhibitor @entity7293 ( @entity7293 , 20 mumol/min for 10 minutes). In six other subjects, @entity452 was infused (6, 10, or 15 micrograms.kg-1.min-1) via a peripheral vein. Intracoronary (n = 8) @entity452 infusions increased LV peak +dP/dt by an average of 33 +/- 3%. The intracoronary infusion of @entity7293 had no effect on baseline LV peak +dP/dt, LV systolic or end-diastolic pressures, aortic pressure, or heart rate. The intracoronary infusion of @entity7293 , concurrent with a second infusion of @entity452 , potentiated the +dP/dt response to @entity452 by 30 +/- 10% (P < .04 versus @entity452 alone). The intracoronary infusion of @entity7293 likewise potentiated the +dP/dt response to the peripheral infusion of @entity452 by 37 +/- 18%. CONCLUSIONS: @entity842 produced in the heart attenuates the positive inotropic response to beta-adrenergic stimulation in @entity1 with @entity1002 . NO may contribute to beta-adrenergic @entity6306 in @entity1 with @entity1002 .
