NEURAL MODULATION OF VENTRICULOARTERIAL COUPLING IN CONSCIOUS DOGS

To investigate the role of autonomic reflexes in stroke-work optimizat ion, we studied ventriculoarterial coupling in unanesthetized dogs wit h the autonomic system intact and blocked. Ventricular contractility w as quantified by the slope of the end-systolic pressure-volume relatio n, ventricular elastance (E(es)). Arterial system properties were quan tified by the ratio of end-systolic pressure to stroke volume, arteria l elastance (E(a)). The coupling between left ventricle and arterial s ystem was expressed by the E(a)-to-E(es) ratio. Changes in arterial bl ood pressure during nitroprusside or angiotensin II infusion were used to elicit reflex-mediated influences on ventriculoarterial coupling. With the autonomic system intact, E(es) doubled during nitroprusside i nfusion while E(a) remained unchanged due to reactive vasoconstrictor forces and tachycardia. Consequently, the E(a)-to-E(es) ratio fell 50% from baseline. Angiotensin II infusion increased E(a) 46% but did not significantly change E(es), resulting in a 26% increase in the E(a)-t o-E(es) ratio. In contrast to ventriculoarterial coupling, stroke work was insensitive to changes in afterload, remaining close to its theor etical maximum. After autonomic blockade, E(es) tended to decrease dur ing nitroprusside and increased during angiotensin II infusion in para llel with changes in E(a), so that the E(a)-to- E(es) ratio did not ch ange from baseline as much as it did with the autonomic system intact. Again, the left ventricle maintained nearly 90% of its maximal stroke work. Thus, over a wide range of afterload, stroke work was kept near its theoretical maximum, independent of autonomic neural regulation. These findings suggest that the feedback neural regulation to restore normal arterial pressure could augment the variability of ventriculoar terial coupling condition when vascular responsiveness to the barorefl exes is limited by vasoactive agents.