摘要
目的:探讨一氧化氮(NO)对肾缺血再灌注(ischem ia-reperfusion in jury,I-R I)时大鼠肾小球超微结构及负电荷位点的影响。方法:SD大鼠15只,建立肾缺血再灌注模型,动物随机分为5组:(1)假手术(sham)组(n=6);(2)I-R I组(n=6),缺血前20 m in舌静脉注入生理盐水0.3 mL;(3)SNP+I-R I组(n=6),缺血前20 m in舌静脉注入2.5μg/kg硝普钠(SNP);(4)AG+I-R I组(n=6),缺血前20 m in舌静脉注入10 mg/kg氨基胍(AG);(5)L-NNA+I-R I组(n=6),缺血前20 m in舌静脉注入10 mg/kg L-硝基精氨酸(L-NNA)。以聚乙烯亚胺(PEI)为阳离子探针标记肾小球滤过膜负电荷位点,透射电镜观察肾I-R I对大鼠肾小球超微结构及负电荷位点的影响。结果:(1)sham组电镜下见肾小球结构正常,肾小球基底膜(GBM)外透明层负电荷位点(AS)清晰,呈连续的规则点线状排列[(19.3±1.7)个/1 000 nm]。I-R I组肾小球足细胞足突有明显的融合现象;GBM外透明层AS排列稀疏[(16.6±1.0)个/1 000 nm,P<0.05],PEI颗粒小。(2)与I-R I组相比,给予SNP使肾I-R I大鼠肾小球滤过膜上皮细胞足突融合现象加重,肾小球GBM的AS[(11.7±3.2)个/1 000 nm]显著少于假手术组(P<0.05),且PEI颗粒的电子致密度也明显低于假手术组;而AG的应用使I-R I大鼠肾小球滤过膜损伤减轻,可见清晰的足突间隙;L-NNA+I-R I组大鼠肾小球上皮细胞足突融合也明显加重,但和I-R I组相比,L-NNA+I-R I组大鼠GBM的AS数量[(14.7±0.9)个/1 000 nm]无显著差异(P>0.05)。结论:肾I-R I时出现肾小球上皮细胞足突融合、肾小球滤过膜的负电荷位点减少等病理性损伤,NO可加重这些损伤;肾I-R I时肾小球滤过膜超微结构的损伤与NO的生成及其作用有关。
AIM ： To investigate the effects of nitric oxide on ultrastructure and anionic sites of glomerular in renal ischemia reperfusion injured （ I - RI ） rats. METHODS ： Animals were divided randomly into five groups ： （ 1 ） sham group （n =6） ; （2） I - RI group （n =6） , 0. 3 mL normal saline was injected via venae lingualis 20 min before ischemia; （ 3 ） SNP ＋ I - RI group （ n = 6 ）, 2. 5 μg/kg sodium nitroprusside （SNP） was injected via venae lingualis 20 min before ischemia; （4） AG ＋ I - RI group （ n =6） , 10 mg/kg aminoguanidine （AG） was injected via venae lingualis 20 min before ischemia; （ 5 ） L - NNA ＋ I - R1 group （ n = 6 ）, 10 mg/kg N^ω - nitro - L - arginine （ L - NNA ） was injected via venae lingualis 20 min before ischemia. Anionic sites of glomerular were studied with a cationic probe - polyethyleneimine （ PEI ） and ultrastructure was observed under electron microscope in renal I - RI rats. RESULTS ： （ 1 ） Ultrastructure of glomerular was normal and anionic sites （AS） was located clearly in lamina rare externa of GBM in sham rats. The PEI particles arranged regularly in line （ 19. 3 ± 1.7/1 000 nm） under electronic microscope. Obvious foot processes derangement and effacement were observed and the AS number in GBM of I - RI group was fewer （ 16. 6 ± 1.0/1 000 nm, P 〈0.05 ） and the particle was smaller than that in sham group. （2） Compared with I - RI group, the foot process effacement was aggravated in SNP ＋ I -RI group mad L - NNA ＋ I - RI group. SNP caused the numbers of anionic sites reduced after renal I-RI （ 11. 7 ± 3.2/ 1 000 nm, P 〈0. 05） , and the electronic density of the PEI granule was also reduced. AG lead a increase in anionic site number （17. 8 ± 1.0/1 000 nm, P 〈 0.05 ）, but still fewer than that in sham group （P 〈 0.05 ）. The numbers of anionic sites was not changed in L- NNA ＋ 1 - Bl group （14. 7 ± 0. 9/1 000 nm, P 〉 0. 05 ）. CONCLUSION： Foot process effacement and reduction of anionic sites were present in glomerular filtration membrane in renal I - RI rats. NO aggravated those injuries, indicating that NO plays a role in the ultrastructure damages of glnmerular filtration membrane in I - RI rats.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2006年第11期2142-2145,共4页
Chinese Journal of Pathophysiology
关键词
一氧化氮
肾
再灌注损伤
Nitric Oxide
Kidney
Reperfusion injury.
