PAROXYSMAL HYPERTENSION DUE TO SINOAORTIC BARORECEPTOR DENERVATION IN HUMANS
PAROXYSMAL HYPERTENSION DUE TO SINOAORTIC BARORECEPTOR DENERVATION IN HUMANS
复制标题
DOI：
10.1161/01.hyp.9.3.309
复制
发表时间：
1987-03-01
期刊：
影响因子：
8.3
通讯作者：
AYLWARD, PE
中科院分区：
文献类型：
--
作者：
AKSAMIT, TR;FLORAS, JS;AYLWARD, PE
患者41岁，既往有颈部和纵隔放射史，双侧颈动脉旁路手术后出现严重的高血压、头痛和皮肤潮红。调查显示，发作期间血压和心率有明显的平行波动，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，这些变化是通过微神经摄影技术直接测量的。用苯肾上腺素将静息动脉压从130/88升高到164/100 mm Hg，或用硝普塞将静息动脉压降低到88/56 mm Hg，不会引起心率或交感神经输出活动的反射性改变。相比之下，心脏充盈压力下降与下体负压产生交感神经活动显著增加。这些结果表明动脉压力感受器反射的传入肢完全丧失，但心肺压力感受器反射保留。他们认为颈动脉和主动脉压力感受器都因先前的放疗和手术而受损。尽管动脉压力感受器功能丧失，但患者没有持续性高血压。高血压的发作似乎是由于中央交感神经驱动的自发波动，而不是由动脉压力感受器缓冲，其方式与在窦主动脉去神经动物中所见的相似。
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.