Fracasso M E, Leone R, Cuzzolin L, Del Soldato P, Velo G P, Benoni G
Institute of Pharmacology, University of Verona, Italy.
Agents Actions. 1990 Nov;31(3-4):313-6. doi: 10.1007/BF01997625.
The administration of indomethacin to rats, at the dose of 10 mg/kg once daily for three days, caused a loss of microsomal cytochrome P-450 and cytochrome b5 in the liver, and a fall in drug-metabolizing enzyme activities (i.e. aminopyrine N-demethylase, NADP cyt. c. reductase). Indomethacin also induced intestinal lesions and a significant increase in Clostridium perfringens enterotoxin levels in the feces at 24 hours after both the second and third day of treatment. The above findings suggest that the development of intestinal lesion and the accompanying release of Clostridium perfringens enterotoxin, as well as hepatic enzyme alterations in the rat, result from indomethacin administration. Some of the data in this paper were presented at the Meeting of British Pharmacological Society in Ireland, July 6th-8th, 1988.
以10毫克/千克的剂量每天给大鼠注射吲哚美辛，持续三天，会导致肝脏微粒体细胞色素P - 450和细胞色素b5减少，以及药物代谢酶活性（即氨基比林N - 脱甲基酶、NADP细胞色素c还原酶）下降。吲哚美辛还会引发肠道损伤，并且在治疗的第二天和第三天后24小时，粪便中产气荚膜梭菌肠毒素水平显著升高。上述研究结果表明，大鼠肠道损伤的发生、产气荚膜梭菌肠毒素的伴随释放以及肝脏酶的改变，均是由吲哚美辛给药所致。本文的部分数据已于1988年7月6日至8日在爱尔兰举行的英国药理学会会议上发表。
