Nordström G, Winsö O, Biber B, Hasselgren P O
Department of Surgery, Ostra Sjukhuset, University of Göteborg, Sweden.
Ann Surg. 1990 Jul;212(1):23-9. doi: 10.1097/00000658-199007000-00004.
Hemodynamic and metabolic consequences of a 90-minute period of liver ischemia followed by 120 minutes of reperfusion were studied in rats that were awake during most of the experiment and in rats anesthetized with either pentobarbital (40 mg/kg body weight) or chloralose (30 mg/kg X hour) during the complete length of the experiment. Ischemia was induced by occluding the blood vessels to the left and median liver lobes with a small vascular clamp, which was removed after 90 minutes. Protein synthesis rate was determined by measuring incorporation rate of 14C-leucine into protein in incubated liver slices. At the end of the ischemic period, adenosine triphosphate levels in liver tissue and protein synthesis rate were reduced by 80% to 90%, with no significant differences among groups. During reperfusion, energy levels and protein synthesis rate remained depressed in the anesthetized animals, but improved, although not to normal values, in the awake rats. Hepatic tissue water increased during ischemia, probably reflecting hepatocellular membrane injury. The increase in hepatic tissue water was more pronounced in the chloralose group than in the other groups of rats. During reperfusion hepatic tissue water remained increased in the anesthetized rats but was normalized in the awake group. Mean arterial blood pressure was stable during ischemia and reperfusion in the pentobarbital anesthetized rats, while a progressive decrease in blood pressure during the experiment was noted in the chloralose group. The results suggest that hemodynamic and metabolic responses to liver ischemia and reperfusion can be influenced by anesthetics. Chloralose may be less suitable than pentobarbital for anesthesia when liver ischemia is inflicted.
在大部分实验过程中清醒的大鼠以及在整个实验过程中用戊巴比妥(40毫克/千克体重)或氯醛糖(30毫克/千克·小时)麻醉的大鼠中,研究了90分钟肝脏缺血继以120分钟再灌注后的血流动力学和代谢后果。通过用一个小血管夹夹闭左叶和中叶肝脏的血管来诱导缺血,90分钟后移除血管夹。通过测量14C-亮氨酸掺入孵育肝切片中蛋白质的掺入率来测定蛋白质合成率。在缺血期结束时,肝组织中的三磷酸腺苷水平和蛋白质合成率降低了80%至90%,各实验组之间无显著差异。在再灌注期间,麻醉动物的能量水平和蛋白质合成率仍然降低,但清醒大鼠的这些指标有所改善,尽管未恢复到正常水平。缺血期间肝组织含水量增加,这可能反映了肝细胞膜损伤。氯醛糖组肝组织含水量的增加比其他大鼠组更明显。在再灌注期间,麻醉大鼠的肝组织含水量仍然增加,但清醒组恢复正常。在戊巴比妥麻醉的大鼠中,缺血和再灌注期间平均动脉血压稳定,而氯醛糖组在实验过程中血压逐渐下降。结果表明,麻醉可影响对肝脏缺血和再灌注的血流动力学和代谢反应。当造成肝脏缺血时,氯醛糖可能不如戊巴比妥适合用于麻醉。