Acute Effects of 6ﾟ Head Down Bed Rest on Carotid Baroreflex and Cerebrovascular Hemodynamic in Human

在基础研究的基础上，研究了6小时卧床(6HDBR)和1小时卧床(OBR)对颈动脉压力感受器反射功能和脑循环的急性影响。(1)为了验证颈吸引法评价颈动脉压力感受器功能的可行性，我们通过测量颈动脉吸引法引起的心率和血压的变化来评价颈动脉压力感受器反射敏感性(BRS)，并与传统的苯肾上腺素方法评价的BRS进行了比较。此外，为了揭示压力感受性反射对颈动脉窦压力(CSP)变化的反应特征，我们使用NS方法和改变NS压力变化率(dp/dt)来评估BRS。NS方法与传统的苯肾上腺素方法一样有效地评价了BRS。结果表明，脉压升高是刺激颈动脉压力感受器的一个因素。压力反射…的特点NS法可观察到CSP对dp/dt变化的更多反应，因此BRS与dp/dt呈正相关。(2)为探讨压力感受性反射介导的自主神经参与晕厥的发病机制，采用鞍支撑头高位倾斜的立位应激负荷，观察血流动力学变化。本研究表明，压力感受性反射介导的自主神经机制可能在晕厥立位应激期间维持血压方面起到更大的作用。(3)为探讨压力感受性反射介导的自主神经功能在体位变化时的变化，通过心率和血压变异性频谱分析来评价下体负压立位负荷时自主神经功能的变化。在本研究中，推测心脏迷走神经传出活动在早期是通过抑制压力感受器反射而被抑制的。反射控制使血管运动性交感神经活动在立位应激后3min达到高峰。用NS法评价6HDBR和OBR时颈动脉压力感受性反射功能和脑血管血流动力学的变化如下：(1)6HDBR和OBR期间均可观察到加压素和去甲肾上腺素的下降，这些变化受卧床时间的影响。6HDBR时BRS升高，6HDBR后OBR时BRS下降，基线血压和心率无明显变化。因此，卧床急性期压力感受器反射对体位变化的反应相差6度。(2)压力感受器反射对颈动脉窦压力dp/dt变化的反应在6HDBR和BR期间不变，交感神经活动减弱，副交感神经活动增加。(3)生理盐水刺激颈动脉压力感受性反射引起的脑血管控制在6HDBR和OBR期间无明显变化。在先前的研究中，我们报道了刺激颈动脉压力感受器的脑血管反应依赖于6HDBR延长后平均血压的变化。结论：6HDBR和OBR急性期对心脑血管血流动力学的神经调控不同。较少

The authors studied acute effects of carotid baroreflex function and cerebral circulation during 4 hours 6 Head Down Bed Rest(6HDBR) and 1 hour horizontal bed rest(OBR) after the following basic studies. (1)To examine the neck suction (NS) method of evaluating carotid baroreceptor function, we evaluated carotid baroreceptor reflex sensitivity (BRS) by measuring changes in heart rate and blood pressure induced by the NS method, and compared BRS evaluated by NS method with BRS evaluated by the conventional phenylephrine method. In additon, to reveal the characteristica of baroreflex responce to change in carotid sinus pressure(CSP), we evaluated BRS using the NS method and varying the rate of change in NS pressure(dp/dt). The NS method was shown to be as effective in evaluating BRS as the conventional phenylephrine method. It was shown that an increase in pulse pressure was a factor in stimulating the carotid baroreceptor when the NS method was used. The characteristics of the baroreflex … More response to change in dp/dt of CSP could be observed in the NS method in order that a positive correlation was observed between BRS and dp/dt. (2)To investigated the baroreflex-mediated autonomic mechanisms involved in the pathogenesis of syncope, hemodynamic changes were examined during orthostatic stress loading by saddle support head-up tilt. This study indicated that baroreflex-mediated autonomic mechanisms other than enhancement of vasomotor aipha-adrenergic activity may make a greater contribution to the maintenance of blood pressure during orthostatic stress in syncope. (3)To investigated the changes of baroreflex-mediated autonomic function against posture change, the autonomic activity evaluated by spectral analysis of heart rate and blood pressure variability was examined during orthostatic stress loading by lower body negative pressure. In this study, it was inferred that cardiac vagal efferent activity is inhibited at early stage via inhibition of the baroreflex during. Reflex control results in an exacerbration of vasomotor sympathetic activity which reaches a peak after 3 minutes of orthostatic stress.The changes of carotid baroreflex function and cerebrovascular hemodynamic during 6HDBR and OBR evaluated by NS method were following.(1)The decreasing of vasopressin and norepinepfrine were observed during both 6HDBR and OBR.These changes were effected by term of bed rest. However, BRS was increased during 6HDBR, and was deceased during OBR after 6HDBR with no changes in base line blood pressure and heart rate. Therefore, baroreflex responces to posture chanege in differnce of 6 degrees in acute phase of bed rest. (2)The baroreflex responce to change in dp/dt of carotic sinus pressure unchanged during 6HDBR and BR with the decreasing of sympathetic activity and increasing of parasympathetic activity. (3)The cerebrovascular contol stimulated by carotid baroreflex using NS method unchanged during 6HDBR and OBR.In previous study, we reported that the cerebrovascular responce in stimulation of carotid baroreceptor depends on changing of mean blood pressure after prolonged 6HDBR.In conclusion, the neural controls of cardiovascular and cerebrovascular hemodynamic are different between 6HDBRand OBR in acute phase. Less