This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wang, S. Y. Articles by Tyberg, J. V. Search for Related Content PubMed PubMed Citation Articles by Wang, S. Y. Articles by Tyberg, J. V.

(Circulation. 1995;91:1205-1212.)
© 1995 American Heart Association, Inc.

Articles

Splanchnic Venous Pressure–Volume Relation During Experimental Acute Ischemic Heart Failure

Differential Effects of Hydralazine, Enalaprilat, and Nitroglycerin

Steven Y. Wang, MD; Dante E. Manyari, MD; Nairne Scott-Douglas, MD, PhD; Otto A. Smiseth, MD, PhD; Eldon R. Smith, MD; John V. Tyberg, MD, PhD

From the Division of Cardiology, Departments of Medicine and Medical Physiology, The University of Calgary, Alberta, Canada.

Background Vasodilator drugs have variable effects on veins and arteries. However, direct measurements of their effects on the splanchnic veins, perhaps the most important volume reservoir, have not been reported. We assessed the effect of acute heart failure and the subsequent administration of hydralazine, enalaprilat, and nitroglycerin on the splanchnic venous pressure–volume relation in intact dogs.

Methods and Results Experimental acute ischemic heart failure was induced in 19 splenectomized dogs by microsphere embolization of the left main coronary artery. Embolization was repeated until left ventricular end-diastolic pressure (LVEDP) reached 20 mm Hg and cardiac output decreased by 50%. The splanchnic vascular pressure–volume relation was determined by radionuclide plethysmography during the control stage, after acute heart failure had been established, and after administration of a vasodilator (hydralazine, enalaprilat, or nitroglycerin) at a dose sufficient to reduce mean aortic pressure by approximately 20%. Induction of acute heart failure was associated with a decrease in the splanchnic vascular volume from 100% to 86±2% and an increase in LVEDP from 6±1 to 21±1 mm Hg (P<.001). There was a parallel leftward shift of the splanchnic vascular pressure–volume curve. After the administration of hydralazine, enalaprilat, and nitroglycerin, the splanchnic vascular volumes increased from 86% to 88±3%, 96±3%, and 113±3%, respectively (P=NS, P<.01, and P<.001, respectively, versus heart failure). After drug administration, the LVEDPs were 18±2, 16±1, and 13±1 mm Hg (P=NS, P<.05, and P<.001, respectively, versus heart failure).

Conclusions Acute heart failure was associated with a parallel leftward shift of the splanchnic venous pressure–volume relation (venoconstriction). Splanchnic (systemic) venoconstriction may in part explain the increased LVEDP during acute heart failure by displacement of blood to the central compartment. Subsequently administered enalaprilat and, to a greater degree, nitroglycerin produced splanchnic venodilation, thereby lowering LVEDP. Hydralazine had no significant effect on the splanchnic veins and only a modest effect on LVEDP. In this model, splanchnic capacitance changes appear to modulate change in left ventricular preload.

Key Words: heart failure • imaging • vasodilation • veins • scintigraphy

This article has been cited by other articles:

				K.-L. He, M. Dickstein, H. N. Sabbah, G.-H. Yi, A. Gu, M. Maurer, C.-M. Wei, J. Wang, and D. Burkhoff Mechanisms of heart failure with well preserved ejection fraction in dogs following limited coronary microembolization Cardiovasc Res, October 1, 2004; 64(1): 72 - 83. [Abstract] [Full Text] [PDF]

				K. Uemura, M. Sugimachi, T. Kawada, A. Kamiya, Y. Jin, K. Kashihara, and K. Sunagawa A novel framework of circulatory equilibrium Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2376 - H2385. [Abstract] [Full Text] [PDF]

				A. A. Nekooeian and C. C. Y. Pang Effects of estrogen on venous function in rats with chronic heart failure Am J Physiol Heart Circ Physiol, June 1, 2000; 278(6): H1941 - H1947. [Abstract] [Full Text] [PDF]

				D. J. Blackman, J. A. Morris-Thurgood, J. J. Atherton, G. R. Ellis, R. A. Anderson, J. R. Cockcroft, and M. P. Frenneaux Endothelium-Derived Nitric Oxide Contributes to the Regulation of Venous Tone in Humans Circulation, January 18, 2000; 101(2): 165 - 170. [Abstract] [Full Text] [PDF]

				L. M. Semeniuk, I. Belenkie, and J. V. Tyberg Acute Effects of Toborinone on Vascular Capacitance and Conductance in Experimental Heart Failure Circulation, July 7, 1998; 98(1): 58 - 63. [Abstract] [Full Text] [PDF]

				S. Y. Wang, D. E. Manyari, and J. V. Tyberg Cardiac Vagal Reflex Modulates Intestinal Vascular Capacitance and Ventricular Preload in Anesthetized Dogs With Acute Myocardial Infarction Circulation, August 1, 1996; 94(3): 529 - 533. [Abstract] [Full Text]