Schützer K M, Haglund U, Falk A
Acta Physiol Scand. 1987 Jul;130(3):359-66. doi: 10.1111/j.1748-1716.1987.tb08149.x.
Bacterial infusion in the cat, causing experimental septic shock, induces an early vascular response mainly characterized by pulmonary hypertension and intestinal vasoconstriction. Prostanoids are held to be important mediators of the pulmonary vascular reaction. This study was performed to explore the involvement of prostanoids in the central haemodynamics and the small intestinal vascular reactions in experimental septic shock. Aortic blood pressure was continuously monitored, as were aortic blood flow, the pressure in a. pulmonalis and the small intestinal venous outflow. All cats (n = 24) were given live E. coli (10(10) ml-1) as a continuous intravenous infusion. One series was pretreated with indomethacin, another with UK-38,485, a specific thromboxane A2 synthetase inhibitor, and a third series served as untreated control. The pulmonary hypertensive response was clearly attenuated in the two pretreated series, in fact abolished in the one given UK-38,485. The early intestinal vasoconstriction was eliminated in the two pretreated series. Later during bacteraemia, when untreated and indomethacin-pretreated cats showed intestinal vasoconstriction, UK-38-485-pretreated animals kept intestinal blood flow within the preseptic range. These data suggest that in the cat, thromboxane A2 is the prostanoid mediating the vascular reactions, not only in the lung but also in the small intestine.
给猫注入细菌以引发实验性脓毒性休克，会诱发一种早期血管反应，其主要特征为肺动脉高压和肠道血管收缩。前列腺素被认为是肺血管反应的重要介质。本研究旨在探讨前列腺素在实验性脓毒性休克的中心血流动力学和小肠血管反应中的作用。持续监测主动脉血压、主动脉血流量、肺动脉压力和小肠静脉流出量。所有猫（n = 24）均接受活大肠杆菌（10¹⁰/ml）持续静脉输注。一组用吲哚美辛预处理，另一组用UK - 38,485（一种特异性血栓素A₂合成酶抑制剂）预处理，第三组作为未处理对照。在两个预处理组中，肺动脉高压反应明显减弱，在给予UK - 38,485的那一组中实际上完全消失。在两个预处理组中，早期肠道血管收缩被消除。在菌血症后期，未处理和吲哚美辛预处理的猫出现肠道血管收缩时，UK - 38 - 485预处理的动物的肠道血流量保持在脓毒症前的范围内。这些数据表明，在猫中，血栓素A₂是介导血管反应的前列腺素，不仅在肺中，而且在小肠中也是如此。
