Journal of Applied Physiology, Vol 76, Issue 1 86-90, Copyright © 1994 by American Physiological Society
Mild hemorrhagic shock does not enhance the risk of CD18 blockade to S. aureus skin inoculations
S. S. Sasaki, S. R. Sharar, J. M. Harlan, C. L. Rice and R. K. Winn
Department of Anesthesiology, University of Washington School of Medicine, Seattle 98105.
Monoclonal antibody (MAb) 60.3 recognizes the leukocyte CD18 glycoprotein
and ameliorates much of the injury after hemorrhagic shock in rabbits and
nonhuman primates. This MAb blocks neutrophil emigration and has been shown
to increase the risk of infection after high-dose inoculation of
Staphylococcus aureus into skin. Hemorrhagic shock might also cause an
increased sensitivity to bacterial injections. Therefore, we examined
changes in host sensitivity to subcutaneous injections of 10(5)-10(8)
colony-forming units (CFU) of S. aureus just before shock. Cardiac output
was lowered to 40-45% of baseline by phlebotomy for 1 h. Intravenous saline
or MAb 60.3 (2 mg/kg) treatment immediately preceded resuscitation with the
shed blood. Cefazolin was given intravenously for 3 days, and the animals
were killed after 7 days for analysis of infectious risk by measuring the
incidence and surface area of skin abscess/necrosis. Bacteria injection
resulted in no infections at 10(5) or 10(6) CFU and one abscess/necrotic
region at 10(7) CFU (7% incidence) in the MAb-treated group. However,
injection of 10(8) CFU resulted in more abscesses/necrotic regions in the
MAb- vs. saline-treated group (86 vs. 25%; P < 0.05). The average size
of these lesions was also larger in the MAb-treated group (4.6 +/- 7.1 vs.
0.5 +/- 0.6 cm2; P < 0.001). These results were similar to previously
published results without shock (Sharar et al., Surgery St. Louis
110:213-220, 1991). We conclude that mild hemorrhagic shock does not
enhance the infectious risk of MAb 60.3 after subcutaneous S. aureus
injection.
