MacLellan D G, Shulkes A, Yao C Z, Hardy K J, Thompson J C
Department of Surgery, University of Texas Medical branch, Galveston 77550.
Surg Gynecol Obstet. 1988 May;166(5):441-6.
The role of vagal hyperactivity in the pathogenesis of gastric stress ulceration that occurs after acute trauma to the cervical cord is controversial. We have used a rat model of transection of the cervical cord to induce gastric stress ulceration and to examine the cause of the ulcers. Cervical cord transection did not increase gastric acid output or plasma levels of gastrin or pancreatic polypeptide, either immediately or up to eight hours later. However, gastric stress ulceration showed a time-related increase in ulceration. Vagal stimulation with 2-deoxy-glucose enhanced the gastric acid output in rats with cervical cord transection but failed to change the quantity or characteristics of the gastric ulceration. We conclude that there is no evidence to support the vagal hyperactivity hypothesis in the pathogenesis of gastric stress ulceration after acute cervical cord injury.
迷走神经活动亢进在急性颈髓损伤后发生的胃应激性溃疡发病机制中的作用存在争议。我们使用颈髓横断的大鼠模型来诱导胃应激性溃疡并研究溃疡的成因。颈髓横断后，无论是立即还是长达八小时后，胃酸分泌量、胃泌素或胰多肽的血浆水平均未增加。然而，胃应激性溃疡的溃疡形成呈现出与时间相关的增加。用2-脱氧葡萄糖进行迷走神经刺激可增强颈髓横断大鼠的胃酸分泌，但未能改变胃溃疡的数量或特征。我们得出结论，没有证据支持急性颈髓损伤后胃应激性溃疡发病机制中的迷走神经活动亢进假说。
