Abstract
Summary
Arterial plasma concentrations of PGF2α and 15-keto-PGF2α were determined in sham shock and splanchnic artery occlusion shock dogs. Arterial PGF2α concentrations (expressed as percentage of control) increased significantly in the SAO group when compared to the sham group during postrelease sampling periods. Similarly, 15-keto-PGF2α, a major metabolite of PGF2α also increased significantly in arterial blood in SAO shock. Comparison of 15-keto-PGF2α and PGF2α at each sampling period suggest that the efficiency of 15-hydroxyprostaglandin dehydrogenase is not impaired during SAO shock in the dog. However, the ability of the kidney and other organs to remove 15-keto-PGF2αfrom the circulation during SAO shock does appear to be significantly reduced.
Although the changes in circulating concentrations of PGF2α are significant, the role of the increased prostaglandin is not clearly understood. We found no basis for any toxic effect of the PGF2α nor of any beneficial action. Others, however, have found exogenous PGF2α to improve survival in circulatory shock (17).
The authors are grateful to Drs. J. Brian Smith and M. Silver for the anti-PGF2α antibody used in this study. We are also grateful to Dr. John Pike of the Upjohn Company for a generous supply of prostaglandin. Indomethacin was supplied by Dr. Alexander Scriabine, Merck Institute for Therapeutic Research, West Point, Pa.
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