Journal of Applied Physiology, Vol 48, Issue 6 957-964, Copyright © 1980 by American Physiological Society
Response of pulmonary veins to increased intracranial pressure and pulmonary air embolization
B. T. Peterson, S. E. Grauer, R. W. Hyde, C. Ortiz, H. Moosavi and M. J. Utell
Brain compression with subdural air causes pulmonary hypertension and
noncardiogenic pulmonary edema (A. B. Malik, J. Appl. Physiol.: Respirat.
Environ. Exercise Physiol. 42: 335-343, 1977). To see whether air emboli to
the lungs rather than brain compression caused these findings, anesthetized
dogs received intravenous air infusions, subdural air infusions, or brain
compression from balloons inflated in the subdural space. Subdural air and
intravenous air resulted in similar vascular responses. Pulmonary artery
pressure (Ppa) increased 160% (P less than 0.01) and pulmonary venous
pressure transiently rose 13 +/- 5 Torr (P less than 0.05) without an
increase in left atrial pressure or cardiac output (Q). The end-tidal PCO2
fell 55% (P less than 0.01) and the postmortem weight of the lungs
increased 55% (P less than 0.05). Brain compression with a subdural balloon
instead of air only caused a 20% rise in Ppa and Q without pulmonary edema.
Thus, pulmonary air emboli rather than brain compression accounts for the
edema and pulmonary hypertension caused by subdural air. Catheters in
pulmonary veins and the left atrium showed that air emboli cause transient
pulmonary venous hypertension as well as a reproducible form of
noncardiogenic pulmonary endema.
