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Journal of Applied Physiology, Vol 50, Issue 5 1022-1026, Copyright © 1981 by American Physiological Society
ARTICLES |
A. F. Pirlo, J. L. Benumof and F. R. Trousdale
We measured lobar hypoxic pulmonary vasoconstriction (HPV) caused by both absorption atelectasis (AA) and nitrogen ventilation (N2) during conditions of a) open chest and positive-pressure ventilation (PPV), b) closed chest ad PPV, and c) closed chest and spontaneous ventilation (SV) and compared conditions a with b and b with c. In eight pentobarbital-anesthetized dogs we found that selective hypoxia of the left lower loe (LLL) caused by either AA or N2 resulted in the same percent decrease in the electromagnetically measured LLL blood flow whether the ches was open or closed to whether ventilation was by PPV or SV (range 58.3-65.0%). Whether the chest was open or closed and whether ventilation was by PPV or SV, reexpansion and ventilation of LLL AA with LLL N2 did not change LLL blood flow and indicated that there were no mechanical forces responsible for the decreased LLL AA blood flow. Differences in the degree of hypoxia, magnitude of transpulmonary pressure, and absolute pulmonary vascular pressure between LLL AA and N2 were considered to be minor. We conclude that the mechanism of decreased blood flow to an atelectatic lobe, whether the chest is open or closed and whether ventilation is by PPV or SV, is entirely due to HPV.
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