Jeppsson B, Freund H R, Gimmon Z, James J H, von Meyenfeldt M F, Fischer J E
Surgery. 1982 Jul;92(1):30-5.
A disturbance of cerebral neurotransmitters and an accumulation of octopamine, a putative false neurotransmitter, have been found in patients with uremic encephalopathy who manifest disorientation, somnolence, asterixis, and coma--symptoms also seen in portal systemic encephalopathy (PSE). Altered plasma concentrations of the neutral amino acids (NAAs) and increased blood-brain NAA transport may play a role in PSE, and in the present study plasma amino acid concentrations and blood-brain barrier NAA transport were investigated in rats with acute and chronic uremia. Acute uremia was produced by unilateral nephrectomy and occlusion of the renal artery of the remaining kidney for 70 minutes; the animals were studied 24 hours later. Chronic uremia was produced by unilateral nephrectomy and 70% to 80% devascularization of the remaining kidney; these animals were studied 2 weeks later. Brain uptake was studied with the technique of Oldendorf, and blood and brain amino acids (AAs) were measured. The blood urea nitrogen (BUN) level in rats with acute uremia increased to 108 mg/dl, in rats with chronic uremic 54 mg/dl, and in sham-operated rats 22 mg/dl. In both uremic groups there was a decrease in plasma branched-chain AAs. In the brain these AA levels were normal, while levels of phenylalanine, tyrosine, and histidine were increased in uremic rats.
在患有尿毒症性脑病的患者中发现了大脑神经递质紊乱以及一种假定的假性神经递质章鱼胺的蓄积，这些患者表现出定向障碍、嗜睡、扑翼样震颤和昏迷，这些症状在门体系统性脑病（PSE）中也可见。中性氨基酸（NAA）的血浆浓度改变以及血脑NAA转运增加可能在PSE中起作用，在本研究中，对急性和慢性尿毒症大鼠的血浆氨基酸浓度和血脑屏障NAA转运进行了研究。急性尿毒症通过单侧肾切除并结扎剩余肾脏的肾动脉70分钟产生；24小时后对动物进行研究。慢性尿毒症通过单侧肾切除并使剩余肾脏70%至80%的血管离断产生；2周后对这些动物进行研究。采用奥尔德endorf技术研究脑摄取，并测量血液和脑氨基酸（AA）。急性尿毒症大鼠的血尿素氮（BUN）水平升至108mg/dl，慢性尿毒症大鼠为54mg/dl，假手术大鼠为22mg/dl。在两个尿毒症组中，血浆支链AA均降低。在脑中，这些AA水平正常，而尿毒症大鼠脑中苯丙氨酸、酪氨酸和组氨酸水平升高。
