Arlt Josef, Jahn Holger, Kellner Michael, Ströhle Andreas, Yassouridis Alexander, Wiedemann Klaus
Department of Psychiatry and Psychotherapy, University Hospital Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Neuropeptides. 2003 Dec;37(6):362-8. doi: 10.1016/j.npep.2003.09.006.
Heart rate variability represents a reliable marker to delineate the status of autonomic nervous system (ANS) function and alterations due to stress in vivo. Interestingly, up to now the effects of corticotropin-releasing hormone (CRH), a key regulator of the stress hormone system, upon heart rate variability are not sufficiently described. Hence, we attempted to investigate the ANS-effects of a CRH bolus and the modulatory influences of atrial natriuretic peptide (ANP), one of the most important functional antagonist of CRH actions.
12 healthy male volunteers were administered 100 microg CRH as bolus injection at 15:00. Six randomly chosen subjects received 150 microg ANP dissolved in normal saline and six subjects a normal saline infusion from 14:45 to 15:15. From 13:00 to 17:00 an ECG was recorded and mean heart rate (HR), total power (TP), very low frequency (VLF), low frequency (LF), LF in normalized units (LF [nu]), high frequency (HF) domains and the LF/HF-ratio in the interval from 14:00 to 16:00 were determined.
After administration of CRH a significant increase in HR and a fast reduction of TP were observed, which lasted about 1 h. Based upon spectral domain analyses the sympathetic activity after CRH administration as indicated by LF [nu] increased by 31% (mean location) during saline. Applying ANP this increase was reduced to 19% (mean location). The VLF component, which is considered to be based in part also on sympathetic influences, indicates comparable effect. During saline the VLF after CRH bolus remained largely unchanged, but was reduced to 66% by ANP. Though the vagal activity indicated by the HF component was reduced after CRH, no significant differences emerged between both treatments. The changes of the LF/HF-ratio were pronounced in both groups. During saline this ratio increased by about 111%, during ANP only by 43% (mean location).
Based upon HRV analysis the CRH administration induced sympathotonic effects which were antagonized by ANP. The observed vagal changes were less pronounced and need further investigation. Further studies of autonomic effects by alterations of CRH secretion in depression and anxiety disorder are strongly warranted.
心率变异性是描绘体内自主神经系统（ANS）功能状态及应激引起的改变的可靠标志物。有趣的是，到目前为止，应激激素系统的关键调节因子促肾上腺皮质激素释放激素（CRH）对心率变异性的影响尚未得到充分描述。因此，我们试图研究静脉注射CRH对ANS的影响以及心房利钠肽（ANP）（CRH作用最重要的功能拮抗剂之一）的调节作用。
12名健康男性志愿者于15:00接受100微克CRH静脉推注。随机选择6名受试者静脉输注溶解于生理盐水中的150微克ANP，另外6名受试者于14:45至15:15静脉输注生理盐水。在13:00至17:00记录心电图，并测定14:00至16:00期间的平均心率（HR）、总功率（TP）、极低频（VLF）、低频（LF）、标准化单位的LF（LF [nu]）、高频（HF）域以及LF/HF比值。
静脉注射CRH后，观察到HR显著增加且TP迅速降低，持续约1小时。基于频谱分析，在输注生理盐水期间，CRH给药后由LF [nu]表示的交感神经活动增加了31%（平均位置）。应用ANP后，这种增加降至19%（平均位置）。VLF成分部分也被认为基于交感神经影响，显示出类似的效应。在输注生理盐水期间，静脉推注CRH后的VLF基本保持不变，但ANP使其降低至66%。虽然CRH后由HF成分表示的迷走神经活动降低，但两种治疗之间未出现显著差异。两组中LF/HF比值的变化都很明显。在输注生理盐水期间，该比值增加约111%，在应用ANP期间仅增加43%（平均位置）。
基于心率变异性分析，静脉注射CRH诱导了交感神经兴奋效应，而ANP可对抗这种效应。观察到的迷走神经变化不太明显，需要进一步研究。强烈需要进一步研究抑郁症和焦虑症中CRH分泌改变对自主神经的影响。
