模拟航海运动病Ca^(2+)内流机制探讨  

Discussion about Mechanism of Ca^(2+) Inflow in Rat Model of Simulated Navigation Motion Sickness

作　　者：徐根兴[1] 王琰[1] 董文度[1] 袁驾南[1] 谢培增 金淑仪[2] 姜正林[2] 李建成[2] 庄坚[2] 

机构地区：[1]海军医学高等专科学校细胞生物学研究室,南京210099 [2]南通医学院航海医学研究所,南通226001

出　　处：《海军医高专学报》1998年第2期65-70,共6页

摘　　要：采用正负文交加速度旋转刺激制备大鼠运动病模型，对运动病大鼠大脑皮质、小脑皮质、脑干前庭区脑细胞的Ca2a变化、c－fosmRNA、Fos蛋白、Na+－K+－ATPase、细胞色素氧化酶、碱性磷酸酶等指标进行了观察，对运动病大鼠血浆TXB2、6-keto－PGF1a和心钠素等进行了放射免疫测定。结果表明，大鼠脑细胞Ca2+内流和脑血流减少是诱发运动病的重要因素之一，用脑益嗪处理大鼠以阻滞Ca2+内流和增加脑血流，可减轻运动病大鼠c－fosmANA、Fos蛋白、Na+-K+-AT-Pase、细胞色素氧化酶、碱性磷酸酶、TXB2、6－keto－PGF1a和心钠素的变化。The rats were used as the experimental models of pica induced hy alternating rota-tional stimulation in an accelerator. The changes of Ca2+, c-fos mRNA, Fos protein, Na+-K+-ATPase, CCO, AKP in cerebral cortex, cerebellar cortex and vestibular area of brain stem of rats with motion sickness were observed. The amount of plasma TXB2, 6-keto-PGF1a and cardionatrin were measured by radioimmunoassay. The results suggested that Ca2+ inflow into brain cells and the decrease of cerebral blood flow might be important factors inducing motion sickness. Cinnar-izine was used to treat the rats so that it inhihited Ca2+ inflow. increased cerebral blood flow and diminished the changes of c-fos mRNA, Fos protein, Na+-K+-ATPase, CCO and AKP, TXB2, 6-keto-PGF1a.

关 键 词：运动病 前庭刺激 钙离子 C-FOS基因 脑益嗪 

分 类 号：R835.1[医药卫生—航空、航天与航海医学]