Shortly after beginning an investigation of long-term extracorporeal perfusion in dogs, we were impressed by the number of animals exhibiting postperfusion signs of central nervous system damage. These signs consisted of hemiplegia, skew deviation of the eyes, generalized ataxia, apathy, and apparent blindness. However, these changes were temporary, and by the ninth day after perfusion all such animals had returned to a presumed normal state. Although 16 of 17 consecutive animals perfused for two hours with a plastic disposable bubble-dispersion-type oxygenator * survived, neurologic changes were noted in 50% of the survivors. Gross examination of these animals' brains several weeks later at the time of elective killing disclosed focal areas of infarction. Similar areas of infarction were also noted in animals without clinical signs of central nervous system damage. The possibility of gas, fibrin, or Antifoam A emboli presented itself as a cause of these changes.14 Although Antifoam substances have