Isolating Selected Systems of Central Nervous System Tissue in Culture to Establish Models of Heat and Other Insult Stress-Prevention: Neurological Mechanisms of Heat Injury and Death

摘要

There is a cross-tolerance between oxidative stress and heat stress. Free radicals are the primary noxious agents in oxygen toxicity. We hypothesized that free radicals are the primary noxious agents in heat stroke as well. Our studies in rodents, which examined specific neurochemical changes followig heat exposure, suggested that free radicals are differently generated in brain regions. The authors also demonstrated regional brain change in the content of protaglandins and catecholamines. The authors further observed that there are animals distinguishable by colonic temperature, and that these animals are differentially susceptible to heat stroke. Animals with high unmanipulated temperatures are at greater risk. These same individuals can be characterized by their neurochemical profiles, which retain their class characteristics upon heating. The authors conclude that animals least susceptible to heat stroke are those whose colonic temperatures are below the group mean, and that within this group, there are differences in regional concentrations of superoxide dismutase (SOD), prostaglandins, and catecholamines, and characteristic changes with heating. Pharmacological manipulation of these parameters may allow for the chemical induction of heat tolerance.