Effect of Exogenous Adrenomedullin on the Glutathion Levels of Plasma and Brain Tissue in Neonatal Rat with Hypoxic-Ischemia Reperfusion Brain Damage
- VernacularTitle:外源性肾上腺髓质素对缺氧缺血再灌注脑损伤新生大鼠血浆及脑组织谷胱甘肽表达的影响
- Author:
guo-cheng, XU
;
ben-biao, GUO
;
shuang-gen, MAO
;
ming-xiong, ZHOU
- Publication Type:Journal Article
- Keywords:
hypoxic-ischemia reperfusion damage,brain;
adrenomedullin;
glutathion
- From:Journal of Applied Clinical Pediatrics
1992;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of exogenous adrenomedullin(ADM) on expressions of glutathion in plasma and brain tissue inneonatal rats with hypoxic-ischemia reperfusion brain damage(HIRBD) and the mechanism of action.Methods Fifty-six cases of 7 d SD rats were randomly divided into 4 groups including normal control group(without any treatment),HIRBD group(the model with hypoxia for 2 h and ischemia for 1 h),primed group(abdomen infusion of ADM at 0.5 h before making model,the other was same to the HIRBD group)and treatment group(abdomen infusion of ADM at onces after making model,the other was same to the HIRBD group).The neonatal rats in 4 groups were derived blood and brain tissue after decapitation at either 4 h or 24 h after reperfusion.The levels of gtutathion(GSH) in plasma and brain tissue were determined by using chromatometry.Results In HIRBD group,the affection areas at 24 h after reperfusion enlarged compared with those at 4 h after reperfusion.Meanwhile,the affection of punctiform degeneration or necrosis at 4 h after reperfusion transformed into the affection of lamellar or diffuse degeneration or necrosis at 24 h after reperfusion.The levels of GSH in plasma and brain tissue in HIRBD group at either 4 h or 24 h after reperfusion were significantly lower than that in normal control group(Pa0.05).Meanwhile the pathology score of brain section in primed group and treatment group were significantly lower than that in HIRBD group at either 4 h or 24 h after reperfusion(Pa0.05).Conclusion Exogenous ADM can induce the neuroprotection in HIRBD by adjusting the expression of GSH.
