Abstract
Summary and Conclusions
Acrolein injected into experimental animals by any of several routes produces a condition identical in its clinical and pathological manifestations to that generally accepted as “shock.” By using the intravenous route and relatively large doses in certain animals, it is believed that this picture is the direct result of capillary damage by acrolein or lipoid breakdown products, rather than the result of the liberation of “H” substance or other tissue breakdown protein substances. Studies concerning the development of antibodies to acrolein in the serum of burned animals and individuals are in progress.
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