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人类因窦主动脉压力感受器去神经支配导致的阵发性高血压。

Paroxysmal hypertension due to sinoaortic baroreceptor denervation in humans.

作者信息

Aksamit T R, Floras J S, Victor R G, Aylward P E

出版信息

Hypertension. 1987 Mar;9(3):309-14. doi: 10.1161/01.hyp.9.3.309.

Abstract

A 41-year-old man with a remote history of neck and mediastinal radiation was seen with severe paroxysms of hypertension, headache, and cutaneous flushing after bilateral carotid bypass surgery. Investigation revealed marked parallel fluctuations in blood pressure and heart rate and elevation of plasma norepinephrine to 1164 pg/ml during a paroxysm. We systematically evaluated his arterial and cardiopulmonary baroreceptor reflex function by assessing changes in heart rate, arterial pressure, and efferent muscle sympathetic nerve activity, which was measured directly by the microneurographic technique. Elevating resting arterial pressure from 130/88 to 164/100 mm Hg with phenylephrine or lowering it to 88/56 mm Hg with nitroprusside produced no reflex changes in heart rate or efferent sympathetic nerve activity. In contrast, decreases in cardiac filling pressures with lower body negative pressure produced a marked increase in sympathetic nerve activity. These findings indicate complete loss of the afferent limb of the arterial baroreceptor reflex but preservation of the cardiopulmonary baroreceptor reflex. They suggest that both carotid and aortic baroreceptors were impaired by the previous radiation and surgery. Despite the loss of arterial baroreceptor function, the patient did not have sustained hypertension. The paroxysms of hypertension appear to be due to spontaneous fluctuations in central sympathetic drive not buffered by arterial baroreceptors in a manner similar to that seen in sinoaortic-denervated animals.

摘要

一名41岁男性,有颈部和纵隔放疗史,在双侧颈动脉搭桥手术后出现严重的阵发性高血压、头痛和皮肤潮红。检查发现,发作期间血压和心率明显同步波动,血浆去甲肾上腺素升高至1164 pg/ml。我们通过评估心率、动脉压和传出肌肉交感神经活动的变化,系统地评估了他的动脉和心肺压力感受器反射功能,传出肌肉交感神经活动通过微神经图技术直接测量。用去氧肾上腺素将静息动脉压从130/88 mmHg升高至164/100 mmHg,或用硝普钠将其降至88/56 mmHg,心率或传出交感神经活动均无反射性变化。相反,下体负压导致心脏充盈压降低,交感神经活动显著增加。这些发现表明动脉压力感受器反射的传入支完全丧失,但心肺压力感受器反射保留。这表明双侧颈动脉和主动脉压力感受器均因既往放疗和手术而受损。尽管动脉压力感受器功能丧失,但患者并未出现持续性高血压。高血压发作似乎是由于中枢交感神经驱动的自发波动未被动脉压力感受器缓冲,类似于在去窦弓神经动物中观察到的情况。

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