Shan Z Z, Dai S M, Su D F
Department of Pharmacology, Faculty of Basic Medical Science, Second Military Medical University, People's Republic of China.
J Cardiovasc Pharmacol. 2001 Sep;38(3):427-37. doi: 10.1097/00005344-200109000-00011.
To verify the independent role of the arterial baroreceptor dysfunction involved in target-organ damage in hypertension, sinoaortic denervated (SAD) rats were used as a model of arterial baroreflex (ABR) deficit. SAD, isolated aortic-denervated (AD), and isolated sinus-denervated (SD) rats were instrumented to record blood pressure (BP), heart rate (HR), BP variability (BPV), HR variability (HRV), ABR function control of heart period (ABR-HP), and BP (ABR-BP). Vascular maximum contractile/relaxant function was determined and organ damage was estimated by observation of morphologic changes. Short-term (postoperative 1 week) SAD caused hypertension and tachycardia in rats. Eighteen weeks after operation, BP and HR values in SAD and SD rats were not different from those in sham-operated rats, but AD rats were hypertensive compared with control group. Although 24-h mean BP values of long-term SAD rats were not different from those of sham-operated rats, 24-h BPV of SAD rats was significantly higher than that of sham-operated rats. Arterial baroreflex function in short-term SAD rats was significantly less than in sham-operated rats, whereas in long-term SAD rats, ABR-HP and ABR-BP were higher than those in short-term SAD rats, but were still significantly lower than those in control groups. At postoperative 18 weeks, baroreflex function in SAD and AD rats was significantly less than function in SD and control groups. SBPmax after phenylephrine and DBPmin after nitroprusside were significantly higher in SAD, AD, and SD rats than in control rats. Baroreflex function was negatively correlated to DBPmin and SBPmax in all denervated rats (n = 44). Some morphologic changes were found 18 weeks after denervation in heart, kidney, and small artery in SAD, AD, and SD rats. Baroreflex function in all denervated rats was negatively related to 24-h BPV values. In contrast, 24-h BPV values in SAD, AD, and SD rats were positively related to organ-damage score. A negative correlation between ABR function and end-organ damage score was found. Arterial baroreflex deficit played an independent and important role in organ-damage in SAD rats with significantly elevated 24-h BPV.
为验证动脉压力感受器功能障碍在高血压靶器官损害中所起的独立作用,将去窦弓神经(SAD)大鼠作为动脉压力反射(ABR)缺陷模型。对SAD大鼠、单纯去主动脉神经(AD)大鼠和单纯去窦神经(SD)大鼠进行仪器植入,以记录血压(BP)、心率(HR)、血压变异性(BPV)、心率变异性(HRV)、ABR对心动周期的功能控制(ABR-HP)以及ABR对血压的控制(ABR-BP)。测定血管的最大收缩/舒张功能,并通过观察形态学变化评估器官损害。短期(术后1周)SAD可导致大鼠高血压和心动过速。术后18周,SAD大鼠和SD大鼠的血压和心率值与假手术大鼠无差异,但AD大鼠与对照组相比存在高血压。尽管长期SAD大鼠的24小时平均血压值与假手术大鼠无差异,但SAD大鼠的24小时BPV显著高于假手术大鼠。短期SAD大鼠的动脉压力反射功能明显低于假手术大鼠,而长期SAD大鼠的ABR-HP和ABR-BP高于短期SAD大鼠,但仍显著低于对照组。术后18周,SAD大鼠和AD大鼠的压力反射功能明显低于SD大鼠和对照组。去氧肾上腺素后的收缩压最大值(SBPmax)和硝普钠后的舒张压最小值(DBPmin)在SAD大鼠、AD大鼠和SD大鼠中均显著高于对照大鼠。在所有去神经大鼠(n = 44)中,压力反射功能与DBPmin和SBPmax呈负相关。去神经18周后,在SAD大鼠、AD大鼠和SD大鼠的心脏、肾脏和小动脉中发现了一些形态学变化。所有去神经大鼠的压力反射功能与24小时BPV值呈负相关。相反,SAD大鼠、AD大鼠和SD大鼠的24小时BPV值与器官损害评分呈正相关。发现ABR功能与终末器官损害评分之间呈负相关。在24小时BPV显著升高的SAD大鼠中,动脉压力反射缺陷在器官损害中起独立且重要的作用。