Response of pulmonary veins to increased intracranial pressure and pulmonary air embolization.
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.
D000818:Animals; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D004285:Dogs; D004618:Embolism, Air / Q000503:physiopathology*; D007427:Intracranial Pressure; D010100:Oxygen / Q000097:blood; D011654:Pulmonary Edema / Q000503:physiopathology*; D011655:Pulmonary Embolism / Q000503:physiopathology*; D011667:Pulmonary Veins / Q000503:physiopathology*
D002245:Carbon Dioxide; D010100:Oxygen