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不可逆失血性休克时肠道前列环素和血栓素的生成

Intestinal prostacyclin and thromboxane production in irreversible hemorrhagic shock.

作者信息

Alemayehu A, Sawmiller D, Chou B S, Chou C C

机构信息

Department of Physiology, Michigan State University, East Lansing 48824-1101.

出版信息

Circ Shock. 1987;23(2):119-30.

PMID:3315288
Abstract

Arterial and intestinal venous blood were sampled every hour for measurement of thromboxane B2 (TXB2) and 6-keto-PGF1 alpha, stable metabolites of thromboxane A2 and prostacyclin, respectively, in dogs subjected to hemorrhagic hypotension at 32.8 +/- 1.4 mm Hg for 3 h, followed by reinfusion of the remaining shed blood. Control dogs were treated alike without hypotension. Arterial and intestinal venous TXB2 significantly increased during hypotensive and post-transfusion periods, the venous concentration being significantly higher than the corresponding arterial. The arterial and venous 6-keto-PGF1 alpha increased during hypotension but decreased during post-transfusion periods. Furthermore, arterial and venous TXB2 to 6-keto-PGF1 alpha concentration ratio increased. Intestinal TXB2 release (blood flow X arteriovenous concentration difference) increased progressively, whereas 6-keto-PGF1 alpha release decreased. No significant changes occurred in the control dogs. This study shows an imbalance in intestinal production and release of TXA2 and PGI2, in favor of TXA2 during severe hemorrhagic hypotension and after blood transfusion. The imbalance may contribute to the development of irreversible hemorrhagic shock and reperfusion injury.

摘要

对犬只进行实验,使其处于32.8±1.4毫米汞柱的失血性低血压状态3小时,随后回输剩余的失血,期间每小时采集动脉血和肠静脉血样本,以测量血栓素B2(TXB2)和6-酮-前列环素F1α,它们分别是血栓素A2和前列环素的稳定代谢产物。对照组犬只接受相同处理,但不造成低血压。在低血压期和输血后,动脉血和肠静脉血中的TXB2显著增加,静脉血中的浓度显著高于相应动脉血。动脉血和静脉血中的6-酮-前列环素F1α在低血压期增加,但在输血后减少。此外,动脉血和静脉血中TXB2与6-酮-前列环素F1α的浓度比值增加。肠道TXB2释放量(血流量×动静脉浓度差)逐渐增加,而6-酮-前列环素F1α释放量减少。对照组犬只未出现显著变化。本研究表明,在严重失血性低血压和输血后,肠道中血栓素A2和前列环素的生成和释放失衡,有利于血栓素A2。这种失衡可能导致不可逆失血性休克和再灌注损伤的发生。

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