Anesthetic Influence on Splanchnic Circulation

我们利用教育、科学和文化部的科研补助金调查了1个。PaCO_2变化对内脏循环的影响[j]。2 .挥发性麻醉剂（氟烷、异氟烷和七氟烷）对肝动脉结扎小猎犬肝脏循环和功能的影响；1988年4月至1991年3月用离体灌注大鼠肝模型观察钙通道阻滞剂对肝细胞的保护作用。项目成果总结如下：1。低碳酸血症引起肝动脉血流量减少，但不影响体循环。高碳酸血症期间，门脉血流量和肝总血流量显著增加。尽管肝总血流量增加，但高碳酸血症时吲哚菁绿（ICG）半衰期和血浆ICG清除率比低碳酸血症时要短，提示高碳酸血症时肝功能受到抑制。我们比较了在肝供氧边缘条件下，挥发性麻醉药对肝循环和肝功能的影响。对9只结扎肝动脉的小猎犬分别给予同等麻醉浓度（1.5 MAC）的氟烷、异氟烷和七氟烷。氟烷和七氟烷在肝脏摄氧量方面有显著差异。与氟烷和异氟烷相比，七氟烷的供氧/摄氧比较小，但能保持肝功能。缺氧120 min后再充氧可加重肝细胞损伤，引起肝血管痉挛。血管痉挛可能是钙诱导的血管痉挛，因为尼卡地平预处理可以预防血管痉挛。结论尼卡地平的保护作用可能与血管痉挛的减弱有关。

With Grand-in-Aid for Scientific Research from the Ministry of Education, Science and Culture we investigated 1. the effects of alterations in PaCO_2 on splanchnic circulation, 2. the effects of volatile anesthetics (halothane, isoflurane and sevoflurane) on hepatic circulation and function in the beagle with hepatic artery ligation, and 3. the protective effects of a calcium channel blocker on the hepatocytes by using the isolated perfused rat liver model between April 1988 and March 1991. The results of the project are summarized as follows :1. Hypocapnia caused a decrease in hepatic arterial blood flow without affecting the systemic circulation. There was a significant increase in portal and total hepatic blood flows during hypercapnia. Despite the increase in total hepatic blood flow the half-life of indocyanine green (ICG) and plasma ICG clearance was less during hypercapnia than during hypocapnia, suggesting the depressed hepatic function during hypercapnia.2. We compare the effects of volatile anesthetics on hepatic circulation and function under condition of marginal hepatic oxygen supply. Equi-anesthetic concentrations (1.5 MAC) of halothane, isoflurane, and sevoflurane were administered to nine beagles with ligation of the hepatic artery. There was a significant difference in hepatic oxygen uptake between halothane and sevoflurane. Sevoflurane is accompanied by a smaller oxygen supply/uptake ratio than halothane and isoflurane, while it preserves the hepatic function.3. Reoxygenation after 120 min hypoxia aggravated the hepatocellular injury and elicited vasospasm of the liver. The vasospasm might be due to calcium-induced vasospasm, because it was prevented by nicardipine pretreatment. It was concluded that the protective effects of nicardipine may be related with attenuation of the vasospasm.