Cuzzolin L, Adami A, Crivellente F, Benoni G
Institute of Pharmacology, University of Verona, Italy.
Inflammation. 1997 Aug;21(4):443-50. doi: 10.1023/a:1027322621660.
In the present study the effects of exogenous and endogenous nitric oxide (NO) on intestinal bacteria and on the intestinal tissue integrity have been investigated in healthy rats and in rats receiving bacterial endotoxin (LPS). A segment of jejunum was taken in order to evaluate tissue damage and hematoxylin-eosin staining; microbiological studies were carried out collecting stool samples. Administration of LPS (5 mg kg-1 i.v.) induced a moderate jejunal damage, which was completely prevented by NG-nitro-L-arginine methyl ester (L-NAME), 5 mg kg-1 s.c.), thus suggesting a damage of endogenous NO on the intestinal mucosa; sodium nitroprusside (SNP, 10 mg kg-1 os) reduced significantly jejunal damage induced by LPS. Endogenous NO produced by the administration of LPS resulted to be cytotoxic for all examined aerobic and anaerobic bacteria, while exogenous NO, released from SNP, showed an inhibitory effect only on Entero. faecalis and E. coli growth. From our data, it seems reasonable to conclude that high local levels of NO are required in order to observe jejunal damage and cytotoxic effects on aerobic and anaerobic faecal flora.
在本研究中,已在健康大鼠和接受细菌内毒素(LPS)的大鼠中研究了外源性和内源性一氧化氮(NO)对肠道细菌以及肠道组织完整性的影响。取一段空肠以评估组织损伤并进行苏木精-伊红染色;通过收集粪便样本进行微生物学研究。静脉注射LPS(5 mg kg-1)可引起中度空肠损伤,而皮下注射5 mg kg-1的NG-硝基-L-精氨酸甲酯(L-NAME)可完全预防这种损伤,这表明内源性NO对肠黏膜有损伤作用;硝普钠(SNP,10 mg kg-1口服)可显著减轻LPS诱导的空肠损伤。LPS给药产生的内源性NO对所有检测的需氧菌和厌氧菌均具有细胞毒性,而SNP释放的外源性NO仅对粪肠球菌和大肠杆菌的生长具有抑制作用。根据我们的数据,似乎有理由得出结论,为了观察到空肠损伤以及对需氧和厌氧粪便菌群的细胞毒性作用,需要较高的局部NO水平。