Quality of poststressor rest influences the ulcerative process.

Abstract

Gastric ulceration in rats is exacerbated by allowing a so-called recovery period after exposure to an ulcerogenic stressor. One hypothesis, which has support from pharmacological studies, argues that this effect is brought about by a rebound of parasympathetic activation. We tested this parasympathetic rebound hypothesis by presenting animals with a fear-inducing (sympathetic-activating) conditioned stimulus (CS) after 2 hr of water-restraint stress. Contrary to the hypothesis, presentation of such a CS increased severity of ulceration compared with those animals that did not receive the CS after restraint stress and control animals. These ulceration data favor instead a sustained activation hypothesis for ulceration, whereby presentation of the CS effectively prolonged the length of time during which animals were under stress, thus enhancing the degree of ulceration. Measurement of plasma corticosterone however indicated a negative correlation between adrenocortical activity and degree of gastric ulceration, contrary to that expected by a sustained activation hypothesis. It is suggested that this inconsistency may be because of the activating of a pituitary-endorphinogenic mediated stress analgesia.

Poststress effects of danger and safety signals on gastric ulceration in rats.

“…In addition, punctate danger signals were equally ulcerative as constant danger. This effect is similar to our earlier findings (Overmier et al, 1987). We also observed that punctate inhibitory safety signals caused as much ulceration as continuous danger.…”

“…In a recent study, we (Overmier, Murison, Ursin, & Skoglund, 1987) attempted to differentiate between these two possible explanations. We reasoned that presentations of danger signals (CS for shock) during the rest period after waterrestraint stress should attenuate any trophotropic-type rebound and thus should reduce the ulceration-promoting mechanisms.…”