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Vol. 83, Issue 6, 1962-1967, December 1997
Department of Physiology, University of South Alabama, Mobile, Alabama 36688
Received 17 March 1997; accepted in final form 29 July 1997.
Parker, James C., and Claire L. Ivey.
Isoproterenol attenuates high vascular pressure-induced
permeability increases in isolated rat lungs. J. Appl.
Physiol. 83(6): 1962-1967, 1997.
To separate the
contributions of cellular and basement membrane components of the
alveolar capillary barrier to the increased microvascular permeability
induced by high pulmonary venous pressures (Ppv), we subjected isolated
rat lungs to increases in Ppv, which increased capillary filtration
coefficient
(Kfc) without
significant hemorrhage (31 cmH2O)
and with obvious extravasation of red blood cells (43 cmH2O). Isoproterenol (20 µM)
was infused in one group (Iso) to identify a reversible cellular
component of injury, and residual blood volumes were measured to assess
extravasation of red blood cells through ruptured basement membranes.
In untreated lungs (High Ppv group),
Kfc increased 6.2 ± 1.3 and 38.3 ± 15.2 times baseline during the 31 and 43 cmH2O Ppv states. In Iso lungs, Kfc was 36.2%
(P < 0.05) and 64.3% of that in the
High Ppv group at these Ppv states. Residual blood volumes calculated
from tissue hemoglobin contents were significantly increased by
53-66% in the high Ppv groups, compared with low vascular
pressure controls, but there was no significant difference between High
Ppv and Iso groups. Thus isoproterenol significantly attenuated
vascular pressure-induced Kfc increases at
moderate Ppv, possibly because of an endothelial effect, but it did not
affect red cell extravasation at higher vascular pressures.
pulmonary hypertension; pulmonary edema; mechanical stress failure; capillary filtration coefficient
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