Basic determinants of epicardial transudation
Stewart, R.H.; Rohn, D.A.; Allen, S.J.; Laine, G.A.
American Journal of Physiology 273(3 Pt 2): H1408-H1414
1997
ISSN/ISBN: 0002-9513 PMID: 9321832 Document Number: 478148
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 (J-V,e/A-e). A Plexiglas hemispheric capsule was attached to the left ventricular epicardial surface of anesthetized dogs. J-V,e/A-e 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 mu-l cntdot h-1 cntdot cm-2 cntdot mmHg-1. An osmotic reflection coefficient of 0.9 was calculated from the difference in J-Ve/A-e of 16.5 +- 8.4 mu-l cntdot h-1 cntdot cm-2 between the two solutions. Graded coronary sinus hypertension induced a linear increase in J-V,e/A-e, which was significantly greater in dogs without cardiac lymphatic occlusion than in those with occlusion.