Flynn J T, Bridenbaugh G A, Lefer A M
Am J Physiol. 1976 Mar;230(3):684-90. doi: 10.1152/ajplegacy.1976.230.3.684.
Prostaglandin F2alpha concentrations were determined in hepatic portal venous plasma of dogs during splanchnic artery occlusion (SAO) shock and in nonshock control dogs. Dogs subjected to SAO shock exhibited a dramatic decrease in mean arterial blood pressure and significant increases in portal venous PGF2alpha and amino-nitrogen concentrations, as well as in cathepsin D and MDF activities. Dogs treated with indomethacin prior to SAO shock did not exhibit a significant increase in portal venous PGF2alpha. Indomethacin had no effect on the increase of plasma amino-nitrogen and only slightly reduced portal venous cathepsin D activity during SAO shock. Nevertheless, indomethacin significantly attenuated the severity of the postrelease hypotension observed in SAO shock and diminished the plasma accumulation of MDF. These studies indicate that prostaglandins are released from the splanchnic region during SAO shock and that this release can be prevented by pretreatment with indomethacin. The role of endogenously released prostaglandins in SAO shock is not clear, but the magnitude of the increase warrants further study.
测定了犬在内脏动脉闭塞(SAO)性休克期间肝门静脉血浆中的前列腺素F2α浓度,并与非休克对照犬进行了比较。遭受SAO性休克的犬平均动脉血压显著下降,门静脉PGF2α、氨基氮浓度以及组织蛋白酶D和心肌抑制因子(MDF)活性显著升高。在SAO性休克前用吲哚美辛治疗的犬门静脉PGF2α没有显著升高。吲哚美辛对血浆氨基氮的升高没有影响,并且在SAO性休克期间仅略微降低门静脉组织蛋白酶D活性。然而,吲哚美辛显著减轻了SAO性休克中观察到的再灌注后低血压的严重程度,并减少了MDF的血浆蓄积。这些研究表明,在SAO性休克期间前列腺素从内脏区域释放,并且这种释放可以通过吲哚美辛预处理来预防。内源性释放的前列腺素在SAO性休克中的作用尚不清楚,但升高的幅度值得进一步研究。