摘要
为探讨脑益嗪抗运动病作用机理,采用放射免疫方法和计算机图像分析系统,对运动病组(MSG)和脑益嗪药物预防组(CPG)大鼠血浆TXB2、6KetoPGF1α和小脑毛细血管内皮细胞Na+K+ATPase进行定量测量和分析研究。结果表明CPG大鼠血浆TXB2和6KetoPGF1α显著低于MSG(p<005),而小脑毛细血管内皮细胞Na+K+ATPase活性则明显高于MSG(p<001)。作者认为,血浆TXB2和6KetoPGF1α降低,与脑益嗪阻断血小板和血管内皮细胞Ca2+内流有关。脑内Na+K+ATPase活性升高,可能是因为脑益嗪扩张脑血管、增加脑血流,阻滞Ca2+内流的结果。这些变化可视为脑益嗪抗运动病作用的重要机理。
To study the mechanism of cinnarizine in preventing motion sickness,TXB 2,6 Keto PGF 1α in rats' blood plasma and Na + K + ATPase activity in the endothelial cells of their cerebellar capillary were measured and analysed by a radioactive immunity analyser and a computer image system.The results showed that TXB 2 and 6 Keto PGF 1α in rats' blood plasma in the cinnarizine preventing group(CPG) decreased remarkably,compared with those in the motion sickness group(MSG) ( p<0.05) .The activity of Na + K + ATPase in the endothelial cells of rats' cerebellar capillary in CPG was higher than that in MSG ( p<0.01) .The authors suggest that the lower concentration of TXB 2 and 6 Keto PGF 1α in rats' blood plasma in CPG is closely related to cinnarizine which prevents Ca 2+ from entering into the platelets and into the endothelial cells of blood vessels.The higher activity of Na + K + ATPase in the cerebellum may be caused by cinnarizene which dilates the blood vessels in the brain,increases the blood flow therein,and hinders Ca 2+ from getting into the cerebellum cells.These change are believed to be the important mechanism of how cinnarizine prevents motion sickness.
出处
《生物医学工程学杂志》
EI
CAS
CSCD
北大核心
1998年第2期151-154,共4页
Journal of Biomedical Engineering
基金
中国人民解放军海军后勤部科研基金