摘要
本实验在大鼠小肠缺血再灌注（I/R）损伤模型上观察左族精氨酸（L－Arginine，L-Arg）和左旋硝基精氨酸（L－NNA）对缺血预处理（IPC）和I／R损伤的影响，旨在探讨内皮源性舒张因子/1-氧化氮(endothlium-derivedrelaxingfactor/nitricoxide,EDRF/ND）系统在IPC细胞保护中的作用。结果表明IPC能减轻小肠I/R后血压下降程度（8．3±2．5vs5．6±0．9kPa，P＜0．01），及肠粘膜出血，减少LDH漏出（0．6±0．4vs1．1±0．4U／L），MDA产生（112．9±3．7vs370．1±27.5mmol/g）；明显改善肠道血管床功能，使伊文思兰渗出减少（153．8±36．6vs341．1±429μg/g，P＜0．01），MPO活性下降（24．6±12．8vs79．9±11．5U/g，P＜0．01）。LPC还使血浆NO2含量升高（3．2±1．0vs1．0±0．2μmol/L，P＜0．01），ET水平下降。L－NNA完全消除IP的保护作用，L-Arg则模拟了IPC的保护作用。提示：IPC对I/R损伤小肠有保护作用，EDRF／NO系统的激活参与了这种保护。
To investigate the involvement of EDHF/NO (endothelium - derived relating factor/nifric oxide)system in the mechanism of cellular protection of IPC, the effects of L - Arg and L - NNA on IPC and I/R (ischemia / reperfusion ) injury were observed on the model of intestinal I/R in rat. It was found that IPC attenuated the decrease of systemic blob pressure aher I/R (8. 3 ± 2. 5vs 5. 8 ± 0. 9kpa, P < 0 .01 ) and intestinal mucocal hemorrhage . In the preconditioned animals , plasma LDH and tissue MDA content were significandy lower than that of the I/R group(0.6 ± 0. 2 and 1 12. 9 ± 3. 7vs 1. 1± 0. 4 U/L and 370. 1± 27. 5 nmol/g. d. w., P < 0. 01 ). Evans blue dye content and myeloperovidase activity of intestinal tissue were significantly lower than that in the I/R group (153. 8 ± 36. 6 and 24.6 ± 12. 8vs 341. 1 ± 42.9ug/g. d. w. And 79.9 ± 11. 5U/g. d. w., P < 0. 01 ). It was also found that IPC increased the plasma NO2 content and decraseed the plasma ET level. The protection of IPC was completely abolished by L - NNA and mimicked by L - Arg. Results suggested that IPC protected the intestine from I/R injury and activation of EDRF/NO system is involved in the mechanism of this protective effect.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1997年第6期646-650,共5页
Chinese Journal of Pathophysiology
