Physiologic studies of the pulmonary capillary bed after barium sulfate embolization.

22 anesthetized dogs were given a barium sulfate suspension intravenously in a dose sufficient to double mean pulmonary artery pressure. 10 sec breath-holding carbon monoxide diffusing capacity (D(LCO10)) was measured before and after this standard embolization in each dog. No post-embolic decrease in D(LCO10) was observed. In the study of this apparent paradox, it was found that the potential for further increase in D(LCO10) during exercise remained after embolization. During rest prolongation of breath holding to 60 sec decreased CO absorption significantly more in the embolized than in the nonembolized dogs. While D(LCO10) was not affected by standard barium embolization, oxygen diffusing capacity was clearly decreased. The bronchial collateral circulation did not participate in preventing a D(LCO10) decrease after embolization since surgical interruption of the bronchial circulation did not alter the response to barium. Microscopic examination of lung sections taken after standard embolization showed plugging of precapillary vessels in the 40-50 mu range. These studies suggest that acute precapillary embolic obstruction of vessels of this size interferes remarkably little with CO absorption over short periods of time, probably because of continued CO absorption in portions of the capillary net distal to the sites of impaction. The remarkable anastomotic nature of this capillary network with multiple sources of access possibly provides the anatomic basis for this observation. This study demonstrates a clear dissociation between acute changes in pulmonary vascular resistance and D(LCO10)-both during rest and exercise.