Fuente Mora Cristina, Norcliffe-Kaufmann Lucy, Palma Jose-Alberto, Kaufmann Horacio
Dysautonomia Center, Department of Neurology, New York University School of Medicine, New York, NY, USA.
Exp Physiol. 2015 Nov;100(11):1269-79. doi: 10.1113/EP085340. Epub 2015 Oct 14.
What is the central question of this study? Our goal was to understand the autonomic responses to eating in patients with congenital afferent baroreflex failure, by documenting changes in blood pressure and heart rate with chewing, swallowing and stomach distension. What is the main finding and its importance? Patients born with lesions in the afferent baroreceptor pathways have an exaggerated pressor response to food intake. This appears to be a sympathetically mediated response, triggered by chewing, that occurs independently of swallowing or distension of the stomach. The chewing-induced pressor response may be useful as a counter-manoeuvre to prevent orthostatic hypotension in these patients. Familial dysautonomia (FD) is a rare genetic disease with extremely labile blood pressure resulting from baroreflex deafferentation. Patients have marked surges in sympathetic activity, frequently surrounding meals. We conducted an observational study to document the autonomic responses to eating in patients with FD and to determine whether sympathetic activation was caused by chewing, swallowing or stomach distension. Blood pressure and R-R intervals were measured continuously while chewing gum (n = 15), eating (n = 20) and distending the stomach by percutaneous endoscopic gastrostomy tube feeding (n = 9). Responses were compared with those of normal control subjects (n = 10) and of patients with efferent autonomic failure (n = 10) who have chronically impaired sympathetic outflow. In patients with FD, eating was associated with a marked but transient pressor response (P < 0.0001) and additional signs of sympathetic activation, including tachycardia, diaphoresis and flushing of the skin. Chewing gum evoked a similar increase in blood pressure that was higher in patients with FD than in control subjects (P = 0.0001), but was absent in patients with autonomic failure. In patients with FD, distending the stomach by percutaneous endoscopic gastrostomy tube feeding failed to elicit a pressor response. The results provide indirect evidence that chewing triggers sympathetic activation. The increase in blood pressure is exaggerated in patients with FD as a result of blunted afferent baroreceptor signalling. The chewing pressor response may be useful as a counter-manoeuvre to raise blood pressure and prevent symptomatic orthostatic hypotension in patients with FD.
本研究的核心问题是什么？我们的目标是通过记录咀嚼、吞咽和胃扩张时血压和心率的变化，来了解先天性传入性压力感受器反射衰竭患者进食时的自主神经反应。主要发现及其重要性是什么？出生时传入性压力感受器通路有病变的患者对食物摄入有过度的升压反应。这似乎是一种由咀嚼触发的交感神经介导的反应，其发生独立于吞咽或胃扩张。咀嚼诱发的升压反应可能作为一种对抗措施，用于预防这些患者的体位性低血压。家族性自主神经功能障碍（FD）是一种罕见的遗传性疾病，由于压力感受器反射传入障碍导致血压极不稳定。患者交感神经活动常有明显波动，常在进餐前后出现。我们进行了一项观察性研究，以记录FD患者进食时的自主神经反应，并确定交感神经激活是由咀嚼、吞咽还是胃扩张引起的。在患者咀嚼口香糖（n = 15）、进食（n = 20）以及通过经皮内镜胃造口管喂养使胃扩张（n = 9）时，连续测量血压和R-R间期。将这些反应与正常对照受试者（n = 10）以及传出性自主神经功能衰竭患者（n = 10，其交感神经传出长期受损）的反应进行比较。在FD患者中，进食与明显但短暂的升压反应相关（P < 0.0001），以及交感神经激活的其他表现，包括心动过速、出汗和皮肤潮红。咀嚼口香糖引起类似的血压升高，FD患者的血压升高幅度高于对照受试者（P = 0.0001），但自主神经功能衰竭患者无此反应。在FD患者中，经皮内镜胃造口管喂养使胃扩张未能引发升压反应。结果提供了间接证据表明咀嚼触发交感神经激活。由于传入性压力感受器信号减弱，FD患者的血压升高更为明显。咀嚼升压反应可能作为一种对抗措施，用于升高FD患者的血压并预防症状性体位性低血压。
