模拟失重对离体大鼠肺动脉血管调节功能的影响

目的 研究模拟失重对离体大鼠肺血管调节功能的影响,旨在探讨模拟失重对肺循环的影响和立位耐力降低的发生机制. 方法采用尾部悬吊(TS)大鼠模拟失重生理效应.24只健康雄性Wistar大鼠随机分为对照组、TS 7 d和TS 14 d共3组.采用离体肺灌流技术,利用Power-lab生理系统记录恒流下大鼠肺循环灌注压的变化,并分别于苯肾上腺素(PE)、乙酰胆碱(Ach)和硝普钠(SNP)药物干预后,观察离体肺血管反应性,并计算出肺血管阻力. 结果与对照组相比,TS7 d和TS 14 d大鼠离体肺在恒流灌注下肺动脉压明显降低(F=3.58～20.86,P<0.05或P<0.01),离体大鼠肺动脉血管对PE的收缩反应明显下降,对Ach和SNP的舒张反应明显增强,同时肺血管阻力也相应降低(F=3.56～20.44,P<0.05或P<0.01). 结论尾吊大鼠离体肺血管灌注压降低,血管收缩反应性降低、舒张反应性增强,肺血管阻力减弱,尾吊模拟失重大鼠肺循环血管调节功能减弱,对失重后立位耐力不良有一定的影响.

Effects of simulated microgravity on regulative function of isolated perfused pulmonary arteries in rats

Objective To study the effects of simulated microgravity on regulative function of isolated perfused pulmonary arteries in rats, in order to investigate the mechanism of the changes of pulmonary circulation and poor orthostatic tolerance under simulated microgravity environment.Methods Tail-suspension (TS) rats were used as the animal model to simulate the physiological effects of microgravity. Twenty-four healthy male Wistar rats were randomly divided into 3 groups:control group (CON), TS for 7 d(TS 7 d) and TS14d. The changes of the regulative function of pulmonary arteries to several vasoactive agents were measured by using the perfusion technique of isolated lung and the data were recorded by Powerlab system. Results Compared with the control group, the perfused pressure of the isolated pulmonary arteries decreased significantly in TS 7 d and TS 14 d groups (F=3.58～20.86, P<0.05 or P<0.01), the contractile responses of pulmonary arteries to phenylephrine(PE) declined in TS 14 d, while the vasodilator responses to acetylcholine(Ach) and sodium nitroprusside (SNP) were markedly enhanced. Moreover, pulmonary vascular resistance(PVR) decreased significantly in TS 7d and TS 14 d rats (F= 3.56～20.44, P<0.05 or P<0.01). Conclusion The isolated pulmonary arteries in TS rats under microgravity showsdecreased perfused pressure and contractile response but increased vasodilator responsiveness, while isolated perfusion PVR attenuated. The impaired regulative functions of pulmonary arteries may influence orthostatic intolerance.