Imler M, Schlienger J L, Chabrier G, Comte F
Pathol Biol (Paris). 1984 Apr;32(4):227-32.
In order to make clearer the pathogenesis of hepatic coma, the clinical tolerance of progressive levels of chronic hyperammonemia were studied in the rat. Increases of blood ammonia in the range of 200 to 600 micrograms/dl were produced within 4 weeks by stricture of the portal vein associated with progressive rises in blood urea resulting from reduction of the renal mass and/or addition of urea to the food. The portal stricture produces a collateral circulation allowing a hepatic bypass of portal blood and the ammonia level of this blood is proportional to the amount of circulating and alimentary urea hydrolyzed in the digestive tract. Only the highest hyperammonemias were associated with decreased nocturnal locomotion of the rats and decrease in the growth rate. The latter was correlated with the ammonia levels. No animal presented signs of coma. These results suggest a good cerebral tolerance by the rat of important chronic hyperammonemias which however seem to have an anorexic effect.
为了更清楚地了解肝昏迷的发病机制,对大鼠慢性高氨血症进行了逐步研究,观察其临床耐受性。通过门静脉狭窄在4周内使血氨升高至200至600微克/分升,同时因肾质量减少和/或在食物中添加尿素导致血尿素逐步升高。门静脉狭窄产生侧支循环,使门静脉血绕过肝脏,该血液中的氨水平与在消化道中水解的循环和食物尿素量成正比。只有最高水平的高氨血症与大鼠夜间活动减少和生长速率降低有关。后者与氨水平相关。没有动物出现昏迷迹象。这些结果表明,大鼠对严重慢性高氨血症具有良好的脑耐受性,但高氨血症似乎有厌食作用。