Abstract
AbstractThe ability of neutrophil leukocytes to extravasate into the peritoneal cavity in response to an intraperitoneal injection of bacterial endotoxin was studied in mice. The normal response of a marked accumulation of intraperitoneal neutrophils was completely abolished by halothane anesthesia. It was further shown that such abolition depended upon the presence of halothane duringthe time the extravasation would normally be occurring. The evidence points toward an effect on either the leukocyte or the vessel rather than a non‐specific “stress” effect. It is suggested that the effect is on the neutrophil, rendering it less deformable and, hence, less able to undergo trans‐vascular diapedesis.
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