Analysis of the cold-water restraint procedure in gastric ulceration and body temperature

Abstract

Gastric mucosal injury induced by body restraint can be enhanced when combined with cold-water immersion. Based on this fact, the present study had two main purposes: (i) to examine the contribution of each of these two forms of stress on the development of gastric ulceration and regulation of body temperature and (ii) to investigate the importance of the animal's consciousness on gastric ulceration induced by the cold-water restraint. Independent groups of animals were exposed for 3 h to one of the following stressful treatments: body restraint plus cold-water (20+1 degrees C) immersion, body restraint alone or cold-water immersion alone. Control animals were not exposed to any form of stress. Half of the animals submitted to each of the four treatments were anesthetized with thionembutal (35 mg/kg), whereas the other half was injected with saline. Results indicated that body restraint alone was not sufficient to induce gastric ulceration or changes in body temperature. On the other hand, cold-water exposure, either alone or in conjunction with body restraint, induced the same amount of stomach erosions and hypothermia. Therefore, it appears that body restraint does not play an important role on gastric ulceration induced by the cold-water restraint procedure. Present results also indicated that conscious and anesthetized animals immersed in cold water presented robust gastric ulceration and a marked drop in body temperature. However, conscious animals developed more severe gastric damage in comparison to anesthetized animals although both groups presented the same degree of hypothermia. These findings suggest that hypothermia resulting from cold-water exposure has a deleterious effect on gastric ulceration but the animal's conscious activity during the cold-water immersion increases the severity of gastric mucosal damage. It is concluded that cold-water restraint is a useful procedure for the study of the underlying mechanisms involved in stress-induced ulceration.