Neural modulation of ventriculoarterial coupling in conscious dogs

• Published in: The American journal of physiology Vol. 266; no. 2 Pt 2; p. H741
• Main Authors: Asanoi, H, Ishizaka, S, Kameyama, T, Sasayama, S
• Format: Journal Article
• Language: English
• Published: United States 01.02.1994
• Subjects: Angiotensin II - pharmacology; Animals; Blood Pressure - drug effects; Coronary Vessels - drug effects; Coronary Vessels - innervation; Coronary Vessels - physiology; Dogs; Heart - drug effects; Heart - innervation; Heart - physiology; Heart Rate - drug effects; Mathematics; Models, Cardiovascular; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - innervation; Muscle, Smooth, Vascular - physiology; Nitroprusside - pharmacology; Pancreatic Elastase - metabolism; Stroke Volume; Systole; Time Factors; Venae Cavae - physiology; Ventricular Function, Left - drug effects; Ventricular Function, Left - physiology
• ISSN: 0002-9513
• DOI: 10.1152/ajpheart.1994.266.2.h741

To investigate the role of autonomic reflexes in stroke-work optimization, we studied ventriculoarterial coupling in unanesthetized dogs with the autonomic system intact and blocked. Ventricular contractility was quantified by the slope of the end-systolic pressure-volume relation, ventricular elastance (Ees). Arterial system properties were quantified by the ratio of end-systolic pressure to stroke volume, arterial elastance (Ea). The coupling between left ventricle and arterial system was expressed by the Ea-to-Ees ratio. Changes in arterial blood pressure during nitroprusside or angiotensin II infusion were used to elicit reflex-mediated influences on ventriculoarterial coupling. With the autonomic system intact, Ees doubled during nitroprusside infusion while Ea remained unchanged due to reactive vasoconstrictor forces and tachycardia. Consequently, the Ea-to-Ees ratio fell 50% from baseline. Angiotensin II infusion increased Ea 46% but did not significantly change Ees, resulting in a 26% increase in the Ea-to-Ees ratio. In contrast to ventriculoarterial coupling, stroke work was insensitive to changes in afterload, remaining close to its theoretical maximum. After autonomic blockade, Ees tended to decrease during nitroprusside and increased during angiotensin II infusion in parallel with changes in Ea, so that the Ea-to-Ees ratio did not change 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.