Costa R S, Rossi M A, Oliveira J S
Br J Exp Pathol. 1979 Dec;60(6):613-9.
A disturbed renal circulation due to an imbalance between vasoconstrictor catecholamines and a vasodilator such as acetylcholine, caused by a decrease in acetylcholine, has been postulated as the basic mechanism of haemorrhagic degeneration of the kidneys in choline deficiency. To explore this hypothesis further a group of male weanling Wistar rats was fed on a choline-deficient diet for 10 days (Group CD). A control group was fed on the same basal diet supplemented with choline (Group CS). Food intake and body weights were registered. The kidneys of choline-supplemented and choline-deficient rats were studied grossly and histologically. The levels of catecholamines (noradrenaline and adrenaline) and acetylcholine were determined. Pathological changes of the kidneys were present in 30 out of 57 choline-deficient rats, permitting the separation of data obtained from deficient rats into those not associated with renal injury (CDa rats) and those associated with renal injury (CDb rats). A marked increase in the levels of renal catecholamines was observed in both CDa and CDb rats. On the other hand, the content of acetylcholine remained unchanged. It is noteworthy that the changes in tissue catecholamine levels occurred before there were changes in kidney weight and morphology. The findings support the concept that an imbalance between sympathetic and parasympathetic systems plays an important role in the pathogenesis of the renal injury of cholinedeficient weanling rats, and that this imbalance would be the result of an excess of catecholamines in the kidneys.
胆碱缺乏时,肾血管收缩性儿茶酚胺与血管舒张剂如乙酰胆碱之间的失衡导致肾循环紊乱,这被认为是肾脏出血性变性的基本机制。为了进一步探讨这一假说,一组雄性断乳Wistar大鼠被给予胆碱缺乏饮食10天(CD组)。一个对照组被给予补充了胆碱的相同基础饮食(CS组)。记录食物摄入量和体重。对补充胆碱和缺乏胆碱的大鼠的肾脏进行大体和组织学研究。测定儿茶酚胺(去甲肾上腺素和肾上腺素)和乙酰胆碱的水平。57只胆碱缺乏大鼠中有30只出现了肾脏病理变化,从而可以将从缺乏胆碱大鼠获得的数据分为与肾损伤无关的(CDa大鼠)和与肾损伤有关的(CDb大鼠)。在CDa和CDb大鼠中均观察到肾脏儿茶酚胺水平显著升高。另一方面,乙酰胆碱含量保持不变。值得注意的是,组织儿茶酚胺水平的变化发生在肾脏重量和形态变化之前。这些发现支持了这样一种观点,即交感神经系统和副交感神经系统之间的失衡在胆碱缺乏断乳大鼠肾损伤的发病机制中起重要作用,并且这种失衡是肾脏中儿茶酚胺过量的结果。