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AJP - Heart and Circulatory Physiology, Vol 264, Issue 5 1624-H1628, Copyright © 1993 by American Physiological Society
ARTICLES |
Y. Han, I. Vergroesen and J. A. Spaan
Department of Medical Physics and Medical Informatics, Faculty of Medicine, University of Amsterdam, The Netherlands.
We measured epicardial lymph pressure (Plymph) in the anesthetized goat (n = 5 goats). To study the transmission of systolic left ventricular pressure (PLV) to Plymph, the effect of an increase in PLV caused by clamping of the descending aorta on Plymph was evaluated. Peak systolic PLV was 131 +/- 4 (+/- SE) mmHg during control (43 beats) and 188 +/- 4 mmHg when elevated due to aortic clamping (157 beats). Peak systolic Plymph was 24.8 +/- 1.0 and 34.8 +/- 1.1 mmHg during control and elevated PLV, respectively. In the first beat of elevated PLV, peak Plymph did not change, although the pressure waveform did. In the subsequent beats, Plymph increased proportionally with increased PLV. When PLV was decreased back to control, Plymph also decreased but did not reach control level until after three beats. The relationship between normalized Plymph and normalized PLV is given by Plymph = 0.70 x PLV + 0.09. The results show that PLV does affect Plymph in a normal beating heart.
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