Murison R, Overmier J B, Glavin G B
Department of Physiological Psychology, University of Bergen, Norway.
Physiol Behav. 1989 Apr;45(4):809-13. doi: 10.1016/0031-9384(89)90299-0.
Temporal patterns of stress and rest have been shown to influence extent of shock-induced pathology. In the present study, the influence of stress-rest cycles was studied on amount of gastric ulceration after two forms of immobilization stress in rats. In Experiment 1, rats were subjected to different patterns of cold supine restraint interspersed with rest periods. A single 180 minute exposure produced more extensive ulceration than did a series of six 30 minute stress periods interspersed with 30 minute rest periods in the home cage. Different results were found in Experiment 2 using the stress of restraint in water and stress/rest patterns parallel to those used in Experiment 1. Previous reports have suggested that a "priming" stress might activate mechanisms protective against gastric ulceration. This was also investigated in Experiment 2 when animals were subjected to either a single 150 minute stress period, a 30 minute priming exposure to the same stressor 150 minutes prior to a 150 minute second exposure, or a 30 minute priming exposure 30 minutes prior to a 150 minute second exposure. No evidence was found for protective effects. In fact, a priming stress 30 minutes prior to final exposure enhanced ulceration. The studies provide some supporting evidence for the role of cycles in determining extent of stress pathology. Such data must be accounted for in any description of the mechanisms of stress-related ulceration.
应激和休息的时间模式已被证明会影响休克诱导的病理程度。在本研究中，研究了应激-休息周期对大鼠两种形式的固定应激后胃溃疡程度的影响。在实验1中，大鼠经历了不同模式的冷仰卧束缚，并穿插有休息期。一次180分钟的暴露比在笼中进行的一系列六个30分钟应激期并穿插30分钟休息期产生了更广泛的溃疡。在实验2中，使用水中束缚应激以及与实验1中使用的应激/休息模式平行的模式，得到了不同的结果。先前的报告表明，“引发”应激可能会激活预防胃溃疡的机制。在实验2中也对此进行了研究，当时动物要么经历一次150分钟的应激期，要么在第二次150分钟暴露前150分钟对同一应激源进行30分钟的引发暴露，要么在第二次150分钟暴露前30分钟进行30分钟的引发暴露。未发现有保护作用的证据。事实上，在最终暴露前30分钟的引发应激增强了溃疡。这些研究为周期在确定应激病理程度中的作用提供了一些支持性证据。在任何关于应激相关溃疡机制的描述中都必须考虑到这些数据。
