Key result
Cardiac lymphatic occlusion blunts coronary sinus hypertension-induced epicardial fluid flux in dogs.
This preclinical study defines the basic determinants of epicardial transudation, demonstrating that coronary sinus hypertension increases epicardial fluid flux, which is modulated by cardiac lymphatic drainage.
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May contribute to epicardial fluid dynamics via venous pressure and lymphatics; leaves open human translation.
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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Stewart et al. (1997) studied Epicardial transudation. Coronary sinus hypertension and cardiac lymphatic obstruction vs. Dogs without cardiac lymphatic occlusion was evaluated on Epicardial fluid flux (JV,e/Ae). Graded coronary sinus hypertension induced a linear increase in epicardial fluid flux, which was significantly greater in dogs without cardiac lymphatic occlusion than in those with occlusion.
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