高血压大鼠视网膜组织Ca2+-ATP酶组织化学及卡托普利终身治疗的观察

目的探讨高血压视网膜病变的发病机制及卡托普利防治高血压视网膜病的治疗机制. 方法 应用光镜定量酶组织化学方法对正常京都种大鼠(正常组),自发性高血压大鼠(高血压组)和卡托普利终身用药治疗的自发性高血压大鼠(用药组)的视网膜组织的Ca2+-ATP酶的分布和活性进行定量观察. 结果 Ca2+-ATP酶在正常组大鼠视网膜组织中主要分布在杆锥细胞层内节、外核层和节细胞神经纤维层,上述三层Ca2+-ATP酶活性(U/μm2)分别为0.662±0.014, 0.665±0.018和0.525±0.021,在高血压组大鼠视网膜组织中,各层Ca2+-ATP酶活性下降,三层Ca2+-ATP酶活性分别为0.610±0.017, 0.598±0.014和0.481±0.010;在用药组大鼠视网膜组织中,Ca2+-ATP酶活性较高血压组增强,三层Ca2+-ATP酶活性分别为0.650±0.016, 0.650±0.014, 0.519±0.022.结论 Ca2+-ATP酶活性下降,细胞内液Ca2+浓度增加是高血压视网膜病变的原因之一;卡托普利防治高血压视网膜病的机制与增强Ca2+-ATP酶和降低细胞内Ca2+浓度有关.

An Enzymic Histochemical Study of Ca2+-ATPase in the Retina of Hypertensive Rats with or without Lifetime Captopril Treatment

Objective\ To explore the mechanisms of retinopathy in SHR and of preventive effect with captopril therapy.\ Methods\ The distribution and activity of Ca 2+ ATPase in the retina of WKY, SHR and SHR having taken lifetime captopril were observed histochemically.\ Results\ The Ca 2+ ATPase in the retina of WKY distributed mostly in the inner segment of rods and cones layer, outer nuclear layer and ganglion layer, the activity of Ca 2+ ATPase was decreased in the retina of SHR, and Ca 2+ ATPase activity was found to be increased in the retina of SHR having taken lifetime captopril compared to SHR.\ Conclusion\ The decrease of Ca 2+ ATPase activity and calcium overload might be one of the important factors relating to retinopathy after hypertension, the increase of activity of Ca 2+ ATPase and the reduction of intracellular calcium might be one factor in the mechanisms relating to the preventive effect of captopril therapy.