摘要
目的：研究运动病大鼠血浆ＴＸＢ２、６－ｋｅｔｏ－ＰＧＦ１α与毛细血管内皮细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶的变化规律及其内在联系，探讨运动病发生的机理。方法：采用放射免疫方法和图像分析系统，对运动病大鼠血浆ＴＸＢ２、６－ｋｅｔｏ－ＰＧＦ１α和小脑毛细血管内皮细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶进行自动检测和定量分析。结果：运动病组大鼠血浆ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α明显高于对照组（Ｐ＜０．０５或Ｐ＜０．０１），而小脑毛细血管内皮细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶的活性则显著低于对照组（Ｐ＜０．０１）。结论：血浆中高浓度的ＴＸＢ２可能是运动病脑血管收缩，脑血流量减少的重要原因之一。脑内Ｎａ＋－Ｋ＋－ＡＴＰ酶活力降低既是脑组织缺血缺氧的结果，又是加重运动病脑血流障碍的继发性原因。
Aim: To study the rule and interrelationship of the changes of plasma TXB-2,6ketoPGF-1α and capillary endothelial cellNa^+K^+-ATPase in rats with motion sickness, so as to explore the pathogenesis of motion sickness. Methods: TXB-2 and 6ketoPGF-1α in rats with motion sickness were measured by radioimmunoassay and the capillary endothelial cell Na+K+ATPase activity in the cerebellum was measured by means of computer image analysis. Results: Blood plasma TXB-2 and 6ketoPGF-1α in the motion sickness group (MSG) were higher than that in the control group (P<0.05 or P<0.01); while the capillary endothelial cell Na^+K^+-ATPase activity in the cerebellum of MSG rats was significantly lower than that of control group(P<0.01). Conclusion: The high concentration of TXB-2 in the blood plasma of the MSG rats might be one of the important causes of contraction of brain vessel and decrease of blood flow. The low Na^+K^+-ATPase activity in the brain tissue is not only the result of brain ischemia and hypoxia, but also the secondary factor aggravating the cerebral blood flow obstruction in motion sicknees.
基金
海军科研基金
关键词
运动病
前列腺素
ATP酶
钠钾
Motion sickness
Prostaglandin Na^+K^+-ATPase
Thromboxane B_2
6ketoPGF-1α
