摘要
目的:观察辣椒素敏感传入神经及内源性一氧化氮(NO)在电刺激PVN减轻大鼠GI-R损伤中的作用.方法:将SD大鼠随机分为6组:GI-R组,假电刺激PVN组,电刺激PVN组,溶剂组,辣椒素预处理组及L-NAME组.采用夹闭大鼠腹腔动脉30min去除动脉夹再灌注1h的GI-R损伤模型.采用核团内电刺激PVN以兴奋其内神经元及大剂量辣椒素预处理使辣椒素敏感传入神经失去功能等方法,研究辣椒素敏感传入神经在PVN对GI-R损伤调控中的作用.结果:用大剂量辣椒素消除辣椒素敏感传入神经作用后,可以部分阻断电刺激PVN引起的保护效应,损伤较电刺激组加重54.85%,与对照组比较差异显著(P<0.05);给予NO合酶阻断剂L-NAME后,能够阻断电刺激PVN的保护效应,损伤较电刺激组加重72.98%,与对照组比较差异显著(P<0.05).结论:辣椒素敏感传入神经及内源性NO参与了电刺激PVN对GI-R损伤的保护效应.
AIM: To elucidate the role of capsaicin-sensitive afferent fibers in mediating the effect of electrical stimulation (ES) of paraventricular nucleus (PVN) against rat gastric ischemia-reperfusion (GI-R) injury.
METHODS: GI-R injury was induced in rats by clamping the celiac artery for 30 min and then reperfusing for 1h. The methods of nuclear electric stimulation to excite the PVN and pretreat- ment with a high dose of capsaicin to ablate the capsaicin-sensitive afferent fibers were used to explore the role of capsaicin-sensitive afferent fibers in the regulation of PVN on GI-R injury.
RESULTS: Pretreament with a high dose of capsaicin to ablate afferent fibers partly abolished the protective effect of PVN against GI-R injury and the injury was increased by 54.85% as compared with that in the PVN stimulation group (P 〈 0.01); Pretreament with L-nitro-L-arginine methyl ester (L-NAME) significantly abolished the protective effect of PVN against GI-R injury and the injury was increased by 72.98% as compared with that in the PVN stimulation group (P 〈 0.01).
CONCLUSION: Capsaicin-sensitive afferent fibers and endogenous NO are involved in the protective effect of PVN stimulation against GI-R injury.
出处
《世界华人消化杂志》
CAS
北大核心
2008年第32期3616-3620,共5页
World Chinese Journal of Digestology
基金
国家自然科学基金资助项目
No. 30570671
徐州医学院院课题基金资助项目
No. 07KJ58~~
关键词
胃缺血-再灌注
室旁核
一氧化氮
辣椒素敏感传入神经
Gastric ischemia-reperfusion
Paraventricular nucleus
Nitric oxide
Capsaicin-sensitive afferent fiber