Murphy C A, Sloan R P, Myers M M
Department of Developmental Psychobiology, Columbia University, Riverside Drive, New York.
J Auton Nerv Syst. 1991 Dec;36(3):237-50. doi: 10.1016/0165-1838(91)90047-7.
The aim of this experiment was to characterize patterns of autonomic control in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats by measuring effects of pharmacologic blockers and using power spectral analysis of heart rate variability (HRV) and blood pressure variability (BPV). Resting HRs and BPs were recorded during a 20-min baseline period and over two 20-min periods of sequential autonomic blockade. On one day, animals received atropine followed by atenolol and on the following day, the drug order was reversed. Power spectrum analyses were performed on 30-s blocks of data throughout each of the three 20-min treatment periods (baseline, single blocker, combined blockade) and HRV and BPV were computed over low and high frequency bands. Increases in HR after atropine were significantly (approx. 40%) smaller in SHR rats than in WKYs. This held true even when animals were pretreated with atenolol. In contrast, decreases in HR following atenolol were similar in the two strains. These results indicate that SHRs have reduced vagal tone, but similar cardiac sympathetic tone compared to WKY rats. Virtually all HRV, over both low and high frequency bands, and in both strains, was inhibited by atropine. SHRs had significantly less high frequency HRV which is consistent with the conclusion that they have reduced cardiac vagal activity when compared with WKYs. BPV was not affected by atropine or atenolol but was inhibited by an alpha-receptor (phentolamine). BPV within both the low and high frequency bands was significantly greater in SHRs, suggesting that sympathetic tone to the vasculature is greater in SHR rats.
本实验的目的是通过测量药理学阻滞剂的作用,并使用心率变异性(HRV)和血压变异性(BPV)的功率谱分析,来表征自发性高血压(SHR)大鼠和正常血压的Wistar-Kyoto(WKY)大鼠的自主神经控制模式。在20分钟的基线期以及两个连续的20分钟自主神经阻滞期记录静息心率和血压。一天,动物先接受阿托品,然后是阿替洛尔,第二天,药物顺序颠倒。在三个20分钟治疗期(基线、单一阻滞剂、联合阻滞)的每一个期间,对30秒的数据块进行功率谱分析,并计算低频和高频带的HRV和BPV。阿托品给药后,SHR大鼠的心率增加幅度(约40%)显著小于WKY大鼠。即使动物先用阿替洛尔预处理,情况依然如此。相反,阿替洛尔给药后两品系大鼠的心率下降情况相似。这些结果表明,与WKY大鼠相比,SHR大鼠的迷走神经张力降低,但心脏交感神经张力相似。实际上,两品系大鼠低频和高频带的所有HRV均被阿托品抑制。SHR大鼠的高频HRV显著较少,这与它们与WKY大鼠相比心脏迷走神经活动降低的结论一致。BPV不受阿托品或阿替洛尔的影响,但被α受体阻滞剂(酚妥拉明)抑制。SHR大鼠低频和高频带的BPV均显著更大,表明SHR大鼠对血管系统的交感神经张力更大。