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首页> 外文期刊>American Journal of Physiology >Role of thromboxane in producing portal hypertension following trauma-hemorrhage.
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Role of thromboxane in producing portal hypertension following trauma-hemorrhage.

机译：血栓烷在创伤性出血后产生门脉高压中的作用。

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摘要

Thromboxane A2 (TXA2) and endothelin-1 (ET-1) have been proposed as the important vasoconstrictors that increase portal venous resistance in paracrine or autocrine fashion. We hypothesized that the hepatic damage following trauma-hemorrhage (T-H) is induced by the impaired hepatic circulation due to the increased production of vasoconstrictors such as ET-1 and TXA2 by the liver. To test this, male Sprague-Dawley rats (n = 6/group) were subjected to trauma (i.e., midline laparotomy) and hemorrhage (35-40 mmHg for 90 min followed by fluid resuscitation) or sham operation. At 2 or 5 h after the end of resuscitation, the liver was isolated and perfused and portal inflow pressure, bile flow, and release of ET-1 and thromboxane B2 (TXB2; a stable metabolite of TXA2) into the perfusate were measured. The level of portal pressure was higher at 5 h following T-H compared with 2 h after T-H and sham. The portal pressure was inversely correlated to the amount of bile production. Furthermore, the bile flow was significantly correlated to the hepatic damage as evidenced by release of lactate dehydrogenase into the perfusate. The level of ET-1 at 5 h following T-H in the perfusate after 30 min of recirculation did not show any difference from sham. However, the levels of TXB2 in the T-H group were significantly higher than those in sham at that interval. These results indicate that the increased release of TXA2 but not ET-1 following T-H might be responsible for producing the increased portal resistance, decreased bile production, and hepatic damage.
机译：血栓烷A2（TXA2）和内皮素1（ET-1）已被建议作为重要的血管收缩剂，以旁分泌或自分泌的方式增加门静脉的抵抗力。我们假设创伤性出血（T-H）后的肝损害是由于肝脏增加的血管收缩剂如ET-1和TXA2的产生而引起的肝循环受损所致。为了测试这一点，对雄性Sprague-Dawley大鼠（每组6只）进行外伤（即中线剖腹手术）和出血（35-40 mmHg持续90分钟，然后进行液体复苏）或假手术。在复苏结束后2或5小时，分离并灌注肝脏，并测量门静脉血流压力，胆汁流量以及ET-1和血栓烷B2（TXB2; TXA2的稳定代谢产物）向灌注液中的释放。 T-H后5 h的门脉压力水平高于T-H和假手术后2 h的门静脉压力水平。门脉压力与胆汁生成量成反比。此外，如乳酸脱氢酶释放到灌注液中所证明的，胆汁流量与肝损害显着相关。循环30分钟后，灌流液中T-H后5小时的ET-1水平与假手术无任何差异。但是，在该时间间隔，T-H组的TXB2水平显着高于假组。这些结果表明，T-H后TXA2释放的增加而不是ET-1的释放可能是造成门静脉阻力增加，胆汁产生减少和肝损害的原因。

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