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作 者:周秀萍[1] 张建福[1] 阎长栋[1] 张咏梅[1]
出 处:《生理学报》2002年第5期435-440,共6页Acta Physiologica Sinica
基 金:ThisworkwassupportedbytheNationalNaturalScienceFoundationofChina (No39970281)andJiangsuProvinceEducationMinistry(No 0 1KJD3 10 0 13 )
摘 要:采用夹闭大鼠腹腔动脉 30min、松开动脉夹血流复灌 6 0min的胃缺血 再灌注损伤 (gastricischemia reperfusioninjury ,GI RI)模型 ,用电和化学刺激、电损毁的方法观察了下丘脑外侧区 (lateralhypothalamicarea ,LHA)对GI RI的影响 ,并对其机制进行了初步分析。结果表明 :(1)以 0 2、0 4、0 6mA的电流强度刺激LHA ,GI RI均显著加重 ,且有强度 效应依赖关系 ;LHA内注射L 谷氨酸 (L Glu)后 ,对GI RI的效应与电刺激相似 ;电损毁双侧LHA ,GI RI面积较电刺激组明显减小 ;(2 )损毁双侧背侧迷走复合体 (dorsalvagalcomplex ,DVC)或切断膈下迷走神经均能取消电刺激LHA加重GI RI的作用 ;(3)电刺激LHA使缺血 再灌注 (ischemia reperfu sion ,I R)的胃粘膜丙二醛 (MDA)含量升高、超氧化物歧化酶 (SOD)活性降低 ;(4)电刺激LHA使I R的胃液量和总酸排出量增多 ;而酸度、胃蛋白酶活性和胃壁结合粘液量等无明显改变。结果提示 :LHA是对GI RI具有加重作用的中枢部位 ,其作用是通过DVC及迷走神经下传的。电刺激LHA加重GI RI的作用与胃粘膜MDA含量增加、SOD活性降低、胃液量和总酸排出量增加等因素有关 ,而似与酸度、胃蛋白酶活性。The effects of electrical and chemical stimulation and electrolytic lesion of lateral hypothalamic area (LHA) on gastric ischemia reperfusion injury (GI RI) were investigated in rats whose celiac arteries were clamped for 30 min and reperfused for 60 min by removal of the clamp. The results are as follows. (1) Electrical stimulation of LHA could aggravate GI RI in an intensity dependent manner by using 0 2, 0 4 or 0 6 mA current respectively. Microinjection of L glutamic acid into LHA resulted in a similar effect to that of electrical stimulation of LHA on GI RI. After electrolytic lesion of bilateral LHA, the area of gastric mucosal injury induced by gastric ischemia reperfusion (GI R) was smaller than that by electrical stimulation of LHA plus GI R. (2) Dorsal vagal complex (DVC) lesion or vagotomy could eliminate the effect of electrical stimulation of LHA on GI RI. (3) Electrical stimulation of LHA increased the content of malondialdehyde (MDA) but decreased the activity of superoxide dismutase (SOD) of ischemia reperfusion (I R) gastric mucosa. (4) Electrical stimulation of LHA plus gastric I R increased gastric juice volume and total acid output, but there were no significant changes in acidity, pepsin activity and gastric barrier mucus. These results indicate that the LHA is an area in the CNS exerting aggravative effects on GI RI. The DVC and vagus may be involved in the regulative effects of LHA on GI RI. These effects are associated with increases in gastric mucosal MDA content, gastric juice volume, and total acid output, and a decrease in SOD activity.Acidity, pepsin activity and gastric barrier mucus do not seem to play an important role.
关 键 词:电刺激 下丘脑外侧区 大鼠 胃缺血-再灌注损伤 孤束核 迷走运动核 迷走神经 丙二醛 超氧化物歧化酶
分 类 号:R33[医药卫生—人体生理学]
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