Machado B H, Brody M J
Department of Pharmacology, University of Iowa, Iowa City 52242.
Hypertension. 1988 Feb;11(2 Pt 2):I135-8. doi: 10.1161/01.hyp.11.2_pt_2.i135.
These studies evaluated the role of the nucleus ambiguus in regulating heart rate and cardiovascular activity. Three days after lesion of the nucleus ambiguus, arterial pressure and heart rate were unchanged; however, subsequent sinoaortic deafferentation produced a significantly greater increase of pressure (156 +/- 4 vs 124 +/- 6 mm Hg) compared to sham lesion. In both groups the heart rate was increased after deafferentation and the intrinsic heart rate (rate seen after autonomic blockade with atropine and propranolol) was significantly reduced. When the sequence was reversed (deafferentation before lesion), pressure (126 +/- 6 vs 126 +/- 7 mm Hg) and heart rate (334 +/- 17 and 340 +/- 16 beats/min) were not altered; however, intrinsic rate fell more. When the nucleus ambiguus was stimulated electrically, two responses emerged: increased pressure without rate changes and increased pressure with bradycardia. These data indicate that 1) lesion of the nucleus ambiguus facilitates hypertension produced by sinoaortic deafferentation unless lesioning follows deafferentation; and 2) stimulation of the nucleus ambiguus produces a pressor effect that is independent of the bradycardic response. We conclude that the nucleus ambiguus may be related to autonomic control of both heart rate and arterial pressure.
这些研究评估了疑核在调节心率和心血管活动中的作用。疑核损伤三天后，动脉血压和心率未发生变化；然而，随后与假手术损伤相比，去主动脉窦神经支配导致压力显著升高（156±4 对 124±6 毫米汞柱）。两组在去神经支配后心率均升高，且固有心率（用阿托品和普萘洛尔进行自主神经阻滞后所见的心率）显著降低。当顺序颠倒（去神经支配在损伤之前）时，压力（126±6 对 126±7 毫米汞柱）和心率（334±17 和 340±16 次/分钟）未改变；然而，固有心率下降更多。当对疑核进行电刺激时，出现了两种反应：压力升高而心率无变化以及压力升高伴心动过缓。这些数据表明：1）疑核损伤会促进去主动脉窦神经支配所产生的高血压，除非损伤在去神经支配之后；2）对疑核的刺激会产生一种与心动过缓反应无关的升压效应。我们得出结论，疑核可能与心率和动脉血压的自主控制有关。
