Pathophysiology and pathogenesis of acute gastric mucosal lesions after hypothermic restraint stress in rats.

The interrelationships of core body temperature, blood viscosity, gastric mucosal blood flow, surface pH of the corpus mucosa, and acute gastric mucosal lesions in rats after up to 3 h of hypothermic stress were investigated. Three groups of rats were studied: (a) control rats restrained at room temperature, (b) conscious rats under restraint and varying degrees of hypothermia, and (c) anesthetized rats under hypothermia. Under hypothermic stress both restrained and anesthetized rats manifested a sharp decline in core temperature, a marked increase in blood viscosity with a mirror-image decrease in gastric mucosal blood flow, a significant decline in gastric mucosal surface pH, and similar frequencies and severities of acute gastric mucosal lesions. In the control group, neither mucosal lesions nor changes in physiologic measurements were observed, except for a decline in mucosal surface pH. An increase in blood viscosity identical to that in rats subjected to hypothermia was observed in vitro when blood temperature was lowered in the viscometer. These findings indicate that hypothermia but not restraint led to an increase in blood viscosity, which in turn resulted in a decrease in mucosal blood flow and the development of gastric mucosal lesions. Also, hyperacidity was found to be a permissive factor in the pathogenesis of mucosal lesions.