Circulation Research, Vol 62, 953-960, Copyright © 1988 by American Heart Association
ARTICLES |
GA Laine
Center for Microvascular, Lymphatic Studies and University of Texas Medical School, Houston 77030.
Changes of myocardial microvascular permeability in chronic renovascular arterial hypertension were studied. Hypertension was induced in dogs utilizing a one-kidney, one-clip Goldblatt model. Systemic arterial pressure, coronary sinus pressure, systemic venous pressure, myocardial lymph flow rate, myocardial interstitial fluid pressure, and the lymph-to-plasma protein concentration ratio for total plasma proteins and for beta-lipoprotein (CL/CP) were determined in control animals and 4-6 weeks following the Goldblatt procedure in hypertensive animals. Control values for the normotensive animals were 123 +/- 17 mm Hg, 7.3 +/- 1.3 mm Hg, 2.5 +/- 2.1 mm Hg, 3.1 +/- 2.1 ml/hr, 14.9 +/- 3.1 mm Hg, 0.82, and 0.33, respectively, while control values for the chronically hypertensive dogs were 160 +/- 20 mm Hg, 7.8 +/- 1.9 mm Hg, 2.9 +/- 2.5 mm Hg, 10.5 +/- 2.5 ml/hr, 24.8 +/- 3.7 mm Hg, 0.87, and 0.31, respectively. Under control conditions, myocardial lymph flow rate was significantly higher in the hypertensive group while no difference could be demonstrated in CL/CP between the two groups. This is indicative of either a change in myocardial microvascular permeability or an increase in microvascular exchange surface area. Coronary sinus pressure was elevated in both groups in order to increase transmicrovascular fluid flux and determine the filtration-independent reflection coefficient (sigma) for each group. Sigma is a surface area-independent indicator of microvascular permeability when determined for specific protein molecules at high transmicrovascular fluid fluxes.(ABSTRACT TRUNCATED AT 250 WORDS)
This article has been cited by other articles:
![]() |
K. V. Desai, G. A. Laine, R. H. Stewart, C. S. Cox Jr., C. M. Quick, S. J. Allen, and U. M. Fischer Mechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edema Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2428 - H2434. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Anand, A. N Mooss, and S. M Mohiuddin Review: Aldosterone Inhibition Reduces the Risk of Sudden Cardiac Death in Patients with Heart Failure Journal of Renin-Angiotensin-Aldosterone System, March 1, 2006; 7(1): 15 - 19. [Abstract] [PDF] |
||||
![]() |
M. Rodriguez-Porcel, J. Herrman, A. R. Chade, J. D. Krier, J. F. Breen, A. Lerman, and L. O. Lerman Long-Term Antioxidant Intervention Improves Myocardial Microvascular Function in Experimental Hypertension Hypertension, February 1, 2004; 43(2): 493 - 498. [Abstract] [Full Text] [PDF] |
||||
![]() |
U. Mehlhorn, H. J. Geissler, G. A. Laine, and S. J. Allen Myocardial fluid balance Eur. J. Cardiothorac. Surg., December 1, 2001; 20(6): 1220 - 1230. [Abstract] [Full Text] [PDF] |
||||
![]() |
U. Mehlhorn, S. J. Allen, D. L. Adams, K. L. Davis, G. R. Gogola, E. R. de Vivie, and G. A. Laine Normothermic Continuous Antegrade Blood Cardioplegia Does Not Prevent Myocardial Edema and Cardiac Dysfunction Circulation, October 1, 1995; 92(7): 1940 - 1946. [Abstract] [Full Text] |
||||
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1988 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |