Journal of Applied Physiology Journal of Neurophysiology
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J Appl Physiol 56: 691-699, 1984;
8750-7587/84 $5.00
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Journal of Applied Physiology, Vol 56, Issue 3 691-699, Copyright © 1984 by American Physiological Society


ARTICLES

Failure of myocardial ischemia to increase pulmonary microvascular permeability in dogs

J. C. Parker, L. Campbell, S. Gilchrist, G. Longenecker and A. E. Taylor

Increased extravascular lung water has been reported following periods of myocardial ischemia. To determine whether increased pulmonary microvascular permeability was produced by ischemia, total protein lymph-to-plasma concentration ratios (CL/CP) were obtained at mechanically increased left atrial pressures (Pla) before and after ligation of the left anterior descending coronary artery in dogs. Pulmonary and systemic vascular pressures and cardiac output were monitored and lymph flow was measured from an afferent tracheobronchial lymphatic. Osmotic reflection coefficients (sigma) for total protein were estimated using CL/CP = 1-sigma at high filtration rates, and permeability-surface area (PSf) products were fit to the data. The postischemic lung lymph data best fit average values of sigma = 0.68 and PSf = 0.073 ml X min-1 X 100 g-1 wet weight. There were no significant differences in lymph protein or water clearances between the pre- and postischemic increased Pla states or for myocardial ischemia compared with control values for the experimental preparation. Levels of 6-ketoprostaglandin F1 alpha, a degradation product of prostacyclin, increased by 10- to 14-fold above preischemic values in pulmonary lymph, and there was a significant increase in pulmonary vascular resistance during ischemia. Extravascular lung water was not increased above that attributed to the increased Pla alone. These data indicate no significant increase in pulmonary microvascular permeability to plasma proteins during myocardial ischemia.





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