Sakio H, Hirose K, Okuda C
Masui. 1989 Feb;38(2):211-5.
Our previous studies indicate that the blockade of the sympathetic nervous system by spinal anesthesia or epidural anesthesia inhibits the release of TXA2 induced by limb ischemia with thigh tourniquet in patients with lower limb surgery. The present study was undertaken to confirm this phenomenon in anesthetized dogs. Twenty one anesthetized dogs underwent 60 min occlusion of the abdominal aorta and the inferior vena cava, followed by reperfusion. They were randomized into three groups: no treatment group and pretreatment groups with either 2 ml of 0.5% bupivacaine intrathecally or 4 mg.kg-1 of labetalol intravenously. In no treatment group plasma TXB2 levels were increased significantly after reperfusion. However, prior treatments with bupivacaine intrathecally or labetalol intravenously inhibited the increases in plasma TXB2 levels after reperfusion. These results suggest that limb ischemia stimulates the TXA2 production, which may be influenced not only by endothelial cell damage and the generation of oxygen free radicals but also by the activation of the sympathetic nervous system.
我们之前的研究表明，在接受下肢手术的患者中，脊髓麻醉或硬膜外麻醉对交感神经系统的阻滞作用可抑制大腿止血带引起的肢体缺血所诱导的血栓素A2（TXA2）释放。本研究旨在在麻醉犬中证实这一现象。21只麻醉犬接受腹主动脉和下腔静脉60分钟的阻断，随后进行再灌注。它们被随机分为三组：未治疗组以及鞘内注射2 ml 0.5%布比卡因或静脉注射4 mg·kg-1拉贝洛尔的预处理组。在未治疗组中，再灌注后血浆TXB2水平显著升高。然而，鞘内注射布比卡因或静脉注射拉贝洛尔进行预处理可抑制再灌注后血浆TXB2水平的升高。这些结果表明，肢体缺血刺激TXA2的产生，这可能不仅受内皮细胞损伤和氧自由基生成的影响，还受交感神经系统激活的影响。
