Imler M, Schlienger J L
J Lab Clin Med. 1979 Dec;94(6):872-8.
It is commonly assumed that the uremia occurring in cirrhotic patients leads to hepatic encephalopathy by means of hyperammonemia produced by bacterial hydrolysis of urea in the digestive tract. Therefore the effect of an increase in circulating urea on portal and systemic blood ammonia levels was investigated in normal rats and in rats with a strictured portal vein. It was shown that moderate chronic uremia, produced by subtotal nephrectomy, significantly increases both portal blood ammonia levels in normal rats and the systemic hyperammonemia resulting from portosystemic shunts in portal-strictured rats. In the latter group, despite a prolonged systemic hyperammonemia of around 400 micrograms/dl, no obvious behavioral modification could be observed, but a significant slowing of the growth rate occurred. This slowing, however, was not correlated with the systemic blood ammonia levels.
通常认为,肝硬化患者发生的尿毒症是通过消化道中尿素经细菌水解产生的高氨血症导致肝性脑病的。因此,研究了循环尿素增加对正常大鼠和门静脉狭窄大鼠门静脉及全身血氨水平的影响。结果表明,通过次全肾切除术产生的中度慢性尿毒症,显著增加了正常大鼠的门静脉血氨水平以及门静脉狭窄大鼠因门体分流导致的全身高氨血症。在后一组中,尽管全身高氨血症持续时间较长,约为400微克/分升,但未观察到明显的行为改变,但生长速度显著减慢。然而,这种减慢与全身血氨水平无关。