The lung serves an important nonrespiratory function by trapping and excreting venous air emboli. The site of trapping and the mechanism of excretion, however, are uncertain. To observe the behavior of bubbles in the pulmonary circulation, we injected venous air emboli into anesthetized dogs and videotaped their elimination from the pulmonary microcirculation by using in vivo microscopy. Small intravenous bubbles lodged exclusively in pulmonary arterioles and were eliminated from that site. To determine whether the gas was dissolving into nearby blood and then was carried to the capillaries for excretion, the rate of bubble radius change was measured during nonperfused conditions produced by balloon occlusion of lobar blood flow and compared with perfused conditions. Bubble volume decreased at the same rate during perfused and nonperfused conditions and thus was independent of regional blood flow. Molecular diffusion of gas directly across the arteriolar wall into alveolar spaces was the most likely mechanism of elimination because calculations based on the Fick equation for molecular diffusion predict an elimination rate nearly identical with those observed experimentally.

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Pulmonary hypertension resulting from venous air embolism is known to increase after ventilation with highly soluble and diffusible gases. Exacerbation of the hypertension could be due to further blockage of the circulation if the bubbles enlarge as a result of ingress of gas by diffusion. This mechanism has been frequently cited but lacks direct proof. To determine directly whether intravascular air bubbles actually enlarge when highly soluble and diffusible gases are inspired, we used microscopy to measure the size of gas emboli in vivo. When air bubbles were injected into the right atrium, the bubbles that appeared in pulmonary arterioles were larger during ventilation with helium or nitrous oxide than with air. Air bubbles injected into the pulmonary artery enlarged when the inspired gas was changed to helium or nitrous oxide. The direction, magnitude, and timing of changes in bubble size were consistent with a net diffusion of gas into the bubbles. These data support the idea that venous air emboli enlarge during ventilation with soluble and diffusible gases and thereby cause further vascular obstruction.

A retrospective analysis of infants with necrotizing enterocolitis was done to evaluate the effects of preoperative abnormalities upon anaesthesia and morlality. Mortality was significantly increased in infants weighing less than 1500 grams (p < .001). Sixty-nine per cent of the infants had hyaline membrane disease and 35 per cent had platelet counts less than 50 • 109 cells/litre (50,000/ram3). Perioperative problems include peritonitis, sepsis, hypovolaemia, acidosis, and prematurity. Other ramifications of prematurity and anaesthesia are discussed.

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