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为验证钾通道开放剂或阻断剂对脑梗塞与左甲状腺素造成损伤是否有益 ,用 MCAO和左甲状腺素造成脑缺血损伤 ,用苄普地尔 ,米诺地尔和格列本脲治疗。左甲状腺素加重 MCAO造成的脑缺血性损害。大鼠给予左甲状腺素 ,1 mg/kg po 1 0 d,而后施行 MCAO(大脑中动脉结扎 )。苄普地尔 ,米诺地尔 ,格列本脲 ,在最后 3 d平行给药 ,左甲状腺素组血清中 T3及 T4分别增加 2 .8倍及 3 .4倍 ( P<0 .0 1 )。药物治疗组 T3,T4亦增多。左甲状腺素组使脑梗塞范围增大 ,格列本脲及苄普地尔组使缩小。氧化应激使 MDA,TXB2 在左甲状腺素组中增多 ( P<0 .0 1 ) ,而减少超氧岐化酶 ( SOD) ,谷胱甘肽过氧化酶 ( GSH-PX)及 6-keto-PGF1α。药物治疗改善上述生化指标。格列本脲的疗效优于米诺地尔。钾通道阻断剂对 MCAO与左甲状腺素形成的脑梗塞损害有明显疗效。
To verify the beneficial effects of potassium channel openers or blockers on cerebral infarction and levothyroxine-induced injury, cerebral ischemia injury was induced by MCAO and levothyroxine, with bepridil, minoxidil, and glyburide . Levothyroxine aggravates cerebral ischemic damage caused by MCAO. Rats were given levothyroxine, 1 mg / kg po for 10 days, followed by MCAO (middle cerebral artery occlusion). Bepridil, minoxidil, and glibenclamide, and the levels of T3 and T4 in levothyroxine serum increased by 2.8 times and 3.4 times (P <0.01) ). Drug treatment group T3, T4 also increased. Levothyroxine group increased the range of cerebral infarction, glibenclamide and bepridil group decreased. Oxidative stress increased the levels of MDA and TXB2 in levothyroxine group (P <0.01), but decreased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and 6-keto -PGF1α. Medication to improve the above biochemical indicators. The efficacy of glyburide is better than that of minoxidil. Potassium channel blockers have a significant effect on cerebral infarction caused by MCAO and levothyroxine.