Xie Yuan-Fang, Jiao Qing, Guo Shu, Wang Fu-Zhen, Cao Ji-Min, Zhang Zheng-Guo
Dept. of Biomedical Engineering, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
J Appl Physiol (1985). 2005 Dec;99(6):2416-22. doi: 10.1152/japplphysiol.00267.2005. Epub 2005 Jul 28.
Stress ulcer is clinically prevalent, but the underlying mechanisms are not well understood. This study aimed to investigate the role of sympathovagal imbalance in the development of water immersion restraint stress (WRS)-induced gastric mucosal lesion. Wistar rats were subjected to either restraint stress (RS) (n = 7) or WRS (n = 7) for 5 h. Linear parameters of heart rate variability and Poincaré plot were analyzed on the basis of the surface ECGs. Gastric mucosal lesion was evaluated by gross anatomy and histology. Mean R-R intervals significantly increased (P < 0.001) in a time-dependent manner in the WRS group but slightly decreased (P < 0.001) in the RS group. Root mean square of successive differences of R-R intervals and high-frequency norm (high-frequency power normalized by the total frequency power) were significantly higher in the WRS group than the RS group (P < 0.001). Low-frequency norm and low-to-high-frequency ratio increased significantly 1 h after stress and then declined to similar levels in both groups. The Poincaré plots of R-R intervals in the WRS group shifted right-upwardly and showed dispersed patterns compared with the RS group. Gastric mucosae showed serious hemorrhage, effusion, and structural collapse in the WRS group but remained normal in the RS group. Bilateral cervical vagotomy suppressed the increase of heart rate variability and prevented the gastric mucosal lesion induced by WRS. We conclude that parasympathetic overactivity is the predominant autonomic response to WRS and is most probably the leading mechanism of WRS-induced gastric mucosal lesion in rat.
应激性溃疡在临床上很常见,但其潜在机制尚未完全明确。本研究旨在探讨交感-迷走神经失衡在水浸束缚应激(WRS)诱导的胃黏膜损伤发生发展中的作用。将Wistar大鼠分为束缚应激组(RS,n = 7)和WRS组(n = 7),分别施加5小时的相应应激。基于体表心电图分析心率变异性的线性参数和庞加莱图。通过大体解剖和组织学评估胃黏膜损伤情况。WRS组的平均R-R间期随时间显著增加(P < 0.001),而RS组则略有下降(P < 0.001)。WRS组的R-R间期连续差值的均方根和高频标准化值(高频功率除以总频率功率)显著高于RS组(P < 0.001)。低频标准化值和低频与高频比值在应激1小时后显著增加,随后两组均降至相似水平。与RS组相比,WRS组的R-R间期庞加莱图向右上方移动并呈现离散模式。WRS组胃黏膜出现严重出血、渗出和结构破坏,而RS组胃黏膜保持正常。双侧颈迷走神经切断术抑制了心率变异性的增加,并预防了WRS诱导的胃黏膜损伤。我们得出结论,副交感神经活动亢进是对WRS的主要自主神经反应,很可能是大鼠WRS诱导胃黏膜损伤的主要机制。