This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted 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 Smiseth, O. A. Articles by Tyberg, J. V. Search for Related Content PubMed PubMed Citation Articles by Smiseth, O. A. Articles by Tyberg, J. V.

Circulation, Vol 76, 875-883, Copyright © 1987 by American Heart Association

ARTICLES

Modulation of vascular capacitance by angiotensin and nitroprusside: a mechanism of changes in pericardial pressure

OA Smiseth, DE Manyari, JA Lima, NW Scott-Douglas, I Kingma, ER Smith and JV Tyberg
University of Calgary, Department of Medicine, Alberta, Canada.

The aim of the present study was to test the hypothesis that vasoactive drugs may modify left ventricular diastolic function by shifting blood between the systemic vascular bed and the heart, thereby changing pericardial and left ventricular pressure. The experiments were done in 10 open-chest, anesthetized, previously splenectomized dogs in which changes in pericardial surface pressure in response to intravenous sodium nitroprusside and angiotensin were related to changes in blood volume in the abdominal region. Blood volume was determined by blood pool scintigraphy (99mTc) and regions of interest were drawn in the liver and in the mesenteric area. Angiotensin was infused at rates that were adjusted to increase mean aortic pressure by 20 and 30 mm Hg, and nitroprusside was infused at rates to decrease mean aortic pressure by 30 and 50 mm Hg. Angiotensin increased pericardial pressure by 3 and 5 mm Hg at the respective doses and there were increments in left ventricular end-diastolic pressure (LVEDP) and left ventricular diameter (sonomicrometry). Angiotensin decreased blood volume in the mesenteric region by 14% and 17%, but did not significantly change blood volume in the liver region. Angiotensin increased portal venous pressure and decreased mesenteric blood volume, suggesting decreased mesenteric venous compliance. Nitroprusside had opposite effects: pericardial pressure was decreased by 5.5 and 6.5 mm Hg by the respective doses. The doses of nitroprusside increased blood volume in the mesenteric region by 14% and 20%, but did not significantly change blood volume in the liver region.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				O. A. Smiseth, K. Russell, and E. W. Remme Pacing in Heart Failure Patients With Narrow QRS: Is There More to Gain Than Resynchronization? Circulation, October 27, 2009; 120(17): 1651 - 1653. [Full Text] [PDF]

				M. A. Perhonen, J. H. Zuckerman, and B. D. Levine Deterioration of Left Ventricular Chamber Performance After Bed Rest : "Cardiovascular Deconditioning" or Hypovolemia? Circulation, April 10, 2001; 103(14): 1851 - 1857. [Abstract] [Full Text] [PDF]

				S. Y. Wang, D. E. Manyari, N. Scott-Douglas, O. A. Smiseth, E. R. Smith, and J. V. Tyberg Splanchnic Venous Pressure–Volume Relation During Experimental Acute Ischemic Heart Failure : Differential Effects of Hydralazine, Enalaprilat, and Nitroglycerin Circulation, February 15, 1995; 91(4): 1205 - 1212. [Abstract] [Full Text]