AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 273: H1408-H1414, 1997;
0363-6135/97 $5.00
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AJP - Heart and Circulatory Physiology, Vol 273, Issue 3 1408-H1414, Copyright © 1997 by American Physiological Society


ARTICLES

Basic determinants of epicardial transudation

R. H. Stewart, D. A. Rohn, S. J. Allen and G. A. Laine
Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station 77843, USA.

Myocardial edema formation, which has been shown to compromise cardiac function, and increased epicardial transudation (pericardial effusion) have been shown to occur after elevation of myocardial venous and lymphatic outflow pressures. The purposes of this study were to estimate the hydraulic conductance and osmotic reflection coefficient for the epicardium and to determine the effect of coronary sinus hypertension and cardiac lymphatic obstruction on epicardial fluid flux (JV,e/Ae). A Plexiglas hemispheric capsule was attached to the left ventricular epicardial surface of anesthetized dogs. JV,e/Ae was determined over 30-min periods for three intracapsular pressures (-5, -15, and -25 mmHg) and two intracapsular solutions exerting colloid osmotic pressures of 7.0 and 2.0 mmHg. Hydraulic conductance was estimated to be 3.7 +/- 0.5 microliters.h-1.cm-2.mmHg-1. An osmotic reflection coefficient of 0.9 was calculated from the difference in JV,e/Ae of 16.5 +/- 8.4 microliters.h-1.cm-2 between the two solutions. Graded coronary sinus hypertension induced a linear increase in JV,e/Ae, which was significantly greater in dogs without cardiac lymphatic occlusion than in those with occlusion.


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R. H. Stewart, H. J. Geissler, S. J. Allen, and G. A. Laine
Protein washdown as a defense mechanism against myocardial edema
Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1864 - H1868.
[Abstract] [Full Text] [PDF]




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