Frink E J, DiGiovanni D A, Davis J R, Brown B R
Department of Anesthesiology, University of Arizona Health Sciences Center, Tucson 85724.
Anesth Analg. 1989 Dec;69(6):776-82.
Elevated serum ammonia may play a role in central nervous system derangement after transurethral resection of the prostate. Glycine used as a surgical irrigant for prostate resection produces ammonia as a by-product after liver and renal metabolism. The presence of liver dysfunction often leads to an inability to remove generated ammonia from the circulation. To determine whether the presence of cirrhosis allows significant metabolism of glycine and the resulting serum ammonia levels generated, the production of ammonia after glycine infusion was examined in normal and cirrhotic rats. Hepatic microsomal enzyme induction was produced in male Sprague-Dawley rats given sodium phenobarbital, added to the drinking water to hasten the development of cirrhosis, by increasing the toxicity of carbon tetrachloride given intragastrically to one group at weekly intervals for production of cirrhosis. A control group was maintained under similar conditions except for carbon tetrachloride dosing. The end point for production of cirrhosis was the development of ascites. Two weeks after the development of ascites in the cirrhotic rats and the discontinuation of phenobarbital in both groups, both control and cirrhotic rats were anesthetized with IP pentobarbital and glycine (1.25 g/kg; 7.5%) was given intravenously. Venous blood samples were taken at intervals up to 120 min for serum ammonia analysis. After the final serum ammonia sample, lethal pentobarbital injection was given and livers and kidneys removed for histologic analysis. Terminal body weight, glycine dose, and renal histology were not different between groups. Liver weights were greater in cirrhotic rats. Baseline serum ammonia levels were also greater int he cirrhotic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
血清氨水平升高可能在经尿道前列腺切除术后中枢神经系统紊乱中起作用。用于前列腺切除的手术灌洗液甘氨酸在肝脏和肾脏代谢后会产生氨作为副产物。肝功能障碍的存在常常导致无法从循环中清除产生的氨。为了确定肝硬化的存在是否会使甘氨酸大量代谢以及由此产生的血清氨水平，在正常大鼠和肝硬化大鼠中检测了输注甘氨酸后的氨生成情况。通过在饮水中添加苯巴比妥钠，对雄性Sprague-Dawley大鼠进行肝微粒体酶诱导，以加速肝硬化的发展，方法是每周给一组大鼠胃内注射四氯化碳以增加其毒性来诱导肝硬化。除了不注射四氯化碳外，对照组在相似条件下饲养。肝硬化形成的终点是腹水的出现。在肝硬化大鼠出现腹水两周后且两组均停用苯巴比妥后，用腹腔注射戊巴比妥麻醉对照组和肝硬化大鼠，并静脉注射甘氨酸（1.25 g/kg；7.5%）。每隔一定时间采集静脉血样直至120分钟，用于分析血清氨。在采集最后一份血清氨样本后，注射致死剂量的戊巴比妥，然后取出肝脏和肾脏进行组织学分析。两组之间的终末体重、甘氨酸剂量和肾脏组织学无差异。肝硬化大鼠的肝脏重量更大。肝硬化大鼠的基线血清氨水平也更高。（摘要截短至250字）
