16-16-dimethylprostaglandin-e2 and Burns

Bacterial translocation and related mortality rates were examined in previously transfused BALB/c mice that were gavaged with 14C radioisotope-labeled Escherichia coli before inflicting a 20% full-thickness flame burn. Radionuclide counts were measured in blood obtained by retro-orbital puncture 4 hours postburn, and survival was recorded for 10 days. Radionuclide counts in the blood correlated well with both radionuclide counts and numbers of viable bacterial in the tissues. Survivors had significantly less bacterial translocation as evidenced by blood radionuclide counts compared with nonsurvivors, and there was a significant inverse correlation between the degree of translocation and the length of survival. In the next experiment, the prostaglandin E (PGE) analogs misoprostol, enisoprost, or 16,16-dimethyl PGE2 were administered to transfused animals for 3 days before burn. Prostaglandin E analogs significantly reduced bacterial translocation as measured by blood radionuclide counts 4 hours postburn and improved survival. The data demonstrate that the intensity of bacterial translocation after burn injury is significantly associated with subsequent death. Improvement of survival by PGE analogs is associated with decreased bacterial translocation.

Topics: 16,16-Dimethylprostaglandin E2; Alprostadil; Animals; Burns; Colony Count, Microbial; Escherichia coli; Female; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; Misoprostol; Prostaglandins E, Synthetic

Burn injuries have been shown to impair immune function. One of the hypotheses for the etiology of the immunosuppression is that burn injuries result in an elevation of prostaglandin E (PGE) levels which then impair leukocyte function. We evaluated the effect of PGE levels on immune function in multiple animal models utilizing T cell subset levels for our immunologic measurements. Elevations in PGE levels were achieved by administering 16,16-dimethyl-prostaglandin E (dPGE) and reductions by administering indomethacin. The animal models included burned rats, burned-septic rats, and nonburned rats. Neither indomethacin nor dPGE administration resulted in alterations of any of the T cell subset populations in our models.

Topics: 16,16-Dimethylprostaglandin E2; Animals; Burns; Disease Models, Animal; Indomethacin; Leukocyte Count; Male; Prostaglandins E, Synthetic; Pseudomonas Infections; Rats; Rats, Inbred Lew; Spleen; T-Lymphocytes; T-Lymphocytes, Helper-Inducer; T-Lymphocytes, Regulatory; Wound Infection