Key result
Intracoronary infusion of the nitric oxide synthase inhibitor L-NMMA reduced vagal inhibition of the dobutamine-stimulated inotropic response by 44-62% in normal dogs.
Why the study?
Does nitric oxide mediate parasympathetic inhibition of beta-adrenergic myocardial contractility in normal dogs?
Does nitric oxide mediate parasympathetic inhibition of beta-adrenergic myocardial contractility in normal dogs?
Effect estimate: 44-62% reduction
p-value: p=<0.001
Nitric oxide plays a role in the normal physiologic regulation of myocardial autonomic responses by mediating vagal inhibition of beta-adrenergic stimulation.
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Supports nitric oxide in canine myocardial autonomic regulation; leaves open translation to human physiology or therapy.
Hare et al. (1995) studied Normal dogs (animal model) (n=18). L-NMMA (NO synthase inhibitor) vs. Baseline (without L-NMMA) was evaluated on Vagal inhibition of dobutamine-stimulated inotropic response (+dP/dt) (44-62% reduction, p=<0.001). Intracoronary infusion of the nitric oxide synthase inhibitor L-NMMA reduced vagal inhibition of the dobutamine-stimulated inotropic response by 44-62% in normal dogs.
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