Key result
Intracoronary infusion of the NO synthase inhibitor L-NMMA potentiated the LV peak +dP/dt response to dobutamine by 30 ± 10% (P<0.04), indicating NO attenuates beta-adrenergic inotropy.
Why the study?
Does NO synthase inhibition with L-NMMA improve the positive inotropic response to dobutamine in patients with left ventricular dysfunction?
Does NO synthase inhibition with L-NMMA improve the positive inotropic response to dobutamine in patients with left ventricular dysfunction?
Effect estimate: 30 +/- 10% potentiation
p-value: p=<0.04
Nitric oxide produced in the heart attenuates the positive inotropic response to beta-adrenergic stimulation in patients with LV dysfunction, suggesting NO contributes to beta-adrenergic hyporesponsiveness.
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NO may contribute to beta-adrenergic hyporesponsiveness in LV dysfunction; leaves open therapeutic NOS inhibition.
Hare et al. (1995) studied Left ventricular dysfunction (n=14). L-NMMA (NO synthase inhibitor) concurrent with dobutamine vs. Dobutamine alone was evaluated on LV peak +dP/dt response (30 +/- 10% potentiation, p=<0.04). Intracoronary infusion of the NO synthase inhibitor L-NMMA potentiated the LV peak +dP/dt response to dobutamine by 30 ± 10% (P<0.04), indicating NO attenuates beta-adrenergic inotropy.
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