Modulation of inflammatory reactions by surgical trauma: lack of relationship with corticosteroid secretion.

The effect of surgery on inflammation was studied in male Wistar R/A rats using the carrageenin-induced edema model. Swelling of the paw was measured in standardized arbitrary units 2, 4, and 6 hr after a subcutaneous injection of carrageenin iota in the subplantar region of the right hind limb. It was significantly depressed in rats submitted to laparotomy (5.0 +/- 0.4, 8.0 +/- 1.0, 13.7 +/- 1.9) when compared with controls simply anesthetized with ether (6.2 +/- 0.5, 15.5 +/- 1.2, 23.7 +/- 0.6) (p less than 0.001 at 4 and 6 hr). This inhibition lasted for at least 24 hr and was also observed after amputation, although in these experiments, the difference between operated animals and controls was not significant. Alterations of the inflammatory cellular infiltrate were studied using polyurethane sponges soaked with carrageenin lambda implanted subcutaneously in control animals and rats undergoing laparotomy or amputation. The total number of cells recovered from these sponges 5 hr after implantation was smaller in operated rats (2.9 +/- 0.4 x 10(6) cells after laparotomy, 3.1 +/- 1.0 x 10(6) cells after amputation) when compared with controls (11.1 +/- 1.9 x 10(6) cells and 10.3 +/- 1.3 x 10(6) cells) (p less than 0.001 for laparotomy and p less than 0.005 for amputation). The inhibitory effect of operative trauma was not abolished by bilateral adrenalectomy performed 12 days before laparotomy. In rats, surgical trauma induces a depression of remote inflammatory reactions. This phenomenon is not related to increased corticosterone levels.