Abstract

Pickrell1 has recently studied experimentally the mechanism involved in the lowered resistance to pneumococcal infections of rabbits following the ingestion of alcohol. He has shown that an induced passive immunity of these animals to intradermal pneumococcal infection is interfered with when stuporous alcoholic intoxication is maintained. He also found deep ether or avertin anesthesia had the same effect as alcoholic intoxication. Because phagocytosis itself was not impaired and the leukocytes were still alive and motile, Pickrell attributed the loss of resistance to a decreased permeability of the capillaries. However, opposed to this theory is the fact that most toxic substances increase capillary permeability. Moreover, alcohol is well known to have the effect of causing dilatation of capillaries. The failure of leukocytic emigration noted by Pickrell may be due to a change in the chemotactic response of the leukocytes themselves rather than to a decreased vascular permeability. The present study, a phase of a general consideration of the mechanisms of lowered resistance to pneumonia,2 is an application of the technic of McCutcheon, Wartman, and Dixon3 to a study of the problems involved. We have compared the response of leukocytes in vitro from alcoholintoxicated rats and normal rats; also of leukocytes from normal human blood and similar leukocytes to which varying amounts of alcohol had been added.

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