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AJP - Heart and Circulatory Physiology, Vol 256, Issue 3 766-H771, Copyright © 1989 by American Physiological Society
ARTICLES |
J. U. Raj, R. Ramanathan, P. Chen and J. Anderson
Department of Pediatrics, University of California, Los Angeles Medical Center, Torrance 90509.
To examine the effects of blood hematocrit (Hct) and apparent viscosity on the pulmonary microcirculation, we studied 30 isolated, perfused 3- to 5-wk-old rabbits with varying perfusate Hct. We partitioned total vascular resistance by measuring pulmonary artery and left atrial pressures and by micropuncture the pressures in the subpleural microcirculation in 20-40 microns diameter arterioles, 20-40 microns venules, and 250-300 microns venules. To prevent active vasomotion and changes in vessel geometry, we paralyzed the vasculature with papaverine hydrochloride. We studied four groups of lungs: group I (n = 7) with low Hct (17.8 +/- 2.4%); group II (n = 9) with medium Hct (46.8 +/- 8.2%); group III (n = 6) with high Hct (74.4 +/- 5.8%); and group IV (n = 8) with both low and high Hct perfusates. Lungs were perfused at constant flow (80 +/- 4 ml.kg body wt-1.min-1) in zone 3, airway and venous pressures being 6 and 8 cmH2O, respectively. We found that in lungs perfused with low Hct, approximately 52% of the total resistance was in arteries, approximately 25% in microvessels, and approximately 21% in small veins, with very little resistance in large veins. With an increase in perfusate hematocrit and apparent viscosity, total pulmonary vascular resistance increased mainly because of an increase in resistance in arteries and small veins, with little change in resistance in microvessels and large veins.
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