SYSTEMIC AND CARDIAC EFFECTS OF NO SYNTHASE INHIBITION ON O₂ DELIVERY AND CONSUMPTION RESPONSES TO DOBUTAMINE

D.J. Penny, J.J. Smolich.

Institute for Reproduction and Development, Monash University; Centre for Heart and Chest Research, Monash Medical Centre, and Department of Medicine, Monash University; Department of Cardiology, Royal Children's Hospital, Melbourne, Victoria.

Although recent evidence suggests that nitric oxide (NO) may inhibit the inotropic actions of b-adrenergic agonists, it is unknown if NO also modulates the effects of these agents on systemic or myocardial oxygen delivery (QO₂) and consumption (MVO₂).  Accordingly, we measured systemic and left ventricular (LV) QO₂ and MVO₂ during dobutamine infusion, before and after inhibition of NO synthase with i.v. N^w-nitro-L-arginine (L-NNA, 25 mk/kg) in 11 anaesthetised ewes instrumented with aortic, pulmonary arterial and coronary sinus catheters, an ultrasonic circumflex coronary artery flow probe and a pulmonary arterial thermistor to measure cardiac output.

Results:  Dobutamine infusion to a peak dose of 10 mg/kg/min increased systemic QO₂ by 59% (P<0.001) and MVO₂ by only 10% (P<0.025), but augmented LV QO₂ by 150% (P<0.001) and MVO₂ by 186% (P<0.001).  L-NNA reduced systemic QO₂ by 19% (P<0.001) but increased MVO₂ by 17% (P<0.02), whereas LV QO₂ and MVO₂ rose by 44% and 50% respectively (both P<0.01).  After L-NNA, dobutamine-induced increases in systemic MVO₂ were 0.49 ml/min/kg higher at any given level of QO₂ compared to dobutamine alone (P<0.001).  however, while dobutamine-related increases in LV QO₂ and MVO₂ were both blunted (P<0.001), the LV QO₂-MVO₂₊ relationship was unaffected by L-NNA.

Conclusions:  These data suggest that NO (1) modulates the coupling between systemic but not myocardial QO₂ and MVO₂ (2) does not influence changes in dobutamine-induced QO₂ supply/demand matching at either site.

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