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为了阐明模拟失重是否引起头部的动脉血管，如基底动脉的收缩反应性增强。方法采用尾部悬吊大鼠模型模拟失重影响，利用离体基底动脉血管环制备测定其对几种血管收缩剂反应性的变化。结果悬吊４ｗｋ组大鼠的基底动脉血管环对ＫＣｌ［（１０～１００）ｍｍｏｌ／Ｌ］、精氨酸加压素［（１０－１５～１０－７）ｍｏｌ／Ｌ］或５羟色胺［（１０－１２～１０－４）ｍｏｌ／Ｌ］的等长收缩反应较同步对照组均显著升高。两组大鼠基底动脉血管环对上述血管收缩剂收缩反应的ＥＣ５０值无显著差别。结论为期４ｗｋ的模拟失重可使大鼠头部的血管，如基底动脉的收缩反应性显著增强。上述结果对“脑血管性晕厥始动机制”假说是一个有力的支持。
In order to elucidate whether simulated weightlessness causes the arterial blood vessels in the head, such as the basilar artery, the contractile response is enhanced. Methods The tail-suspended rat model was used to simulate the effects of weightlessness. The changes of reactivity to several vasoconstrictors were measured by isolated basilar artery vasculature. Results The basilar artery rings of rats in 4wk group were significantly inhibited by KCl [(10-100 mmol / L)], arginine vasopressin [(10-15-10-7) mol / L] or 5-hydroxytryptamine (10-12 ~ 10-4) mol / L] was significantly higher than the synchronous control group were significantly increased. There was no significant difference in the EC50 values of the contractions between the two groups of basilar artery rings in the above vasoconstrictors. Conclusion Simulated weight loss at 4 weeks significantly increases the contractile response of blood vessels in the rat’s head, such as the basilar artery. The above results provide a strong support for the hypothesis of “the initial mechanism of cerebrovascular syncope.”