Chih-Ya Yang1, Mao-Tsun Lin. 1. Institute of Physiology, National Yang-Ming University, Taipei, Taiwan, Republic of China.
Abstract
BACKGROUND AND PURPOSE: Heatstroke is associated with cerebral ischemia as well as increased levels of interleukin-1beta, dopamine, and glutamate in the brain. These factors are known to increase free radical production. This study attempted to ascertain whether an excessive accumulation of cytotoxic free radicals in the brain and oxidative stress can occur during heatstroke. METHODS: Urethane-anesthetized rats underwent instrumentation for the measurement of mean arterial pressure, cerebral blood flow, neuronal damage score, and colonic temperature. Rats were exposed to heat stress (ambient temperature, 42 degrees C) until mean arterial pressure and cerebral blood flow began to decrease from their peak levels, which was arbitrarily defined as the onset of heatstroke. Controlled rats were exposed to 24 degrees C. Concentrations of dihydroxybenzoic acid, lipid peroxidation, rate of O2*- generation, superoxide dismutase, and catalase activity of the brain or other vital organs were assessed during heatstroke. RESULTS: The values of mean arterial pressure and cerebral blood flow after heatstroke onset were all significantly lower than those in control rats. However, the values of colonic temperature, dihydroxybenzoic acid levels in the striatum, and neuronal damage score were greater. The extent of lipid peroxidation in the brain and the rate of O2*- generation in the brain, liver, and heart were all greater in rats after heatstroke onset. In contrast, the values of total superoxide dismutase in the brain, liver, and heart and the catalase activity in the brain were lower. CONCLUSIONS: Taken together, these results indicate that hydroxyl radicals mediate cerebral ischemic injury associated with heatstroke.
BACKGROUND AND PURPOSE:Heatstroke is associated with cerebral ischemia as well as increased levels of interleukin-1beta, dopamine, and glutamate in the brain. These factors are known to increase free radical production. This study attempted to ascertain whether an excessive accumulation of cytotoxic free radicals in the brain and oxidative stress can occur during heatstroke. METHODS:Urethane-anesthetized rats underwent instrumentation for the measurement of mean arterial pressure, cerebral blood flow, neuronal damage score, and colonic temperature. Rats were exposed to heat stress (ambient temperature, 42 degrees C) until mean arterial pressure and cerebral blood flow began to decrease from their peak levels, which was arbitrarily defined as the onset of heatstroke. Controlled rats were exposed to 24 degrees C. Concentrations of dihydroxybenzoic acid, lipid peroxidation, rate of O2*- generation, superoxide dismutase, and catalase activity of the brain or other vital organs were assessed during heatstroke. RESULTS: The values of mean arterial pressure and cerebral blood flow after heatstroke onset were all significantly lower than those in control rats. However, the values of colonic temperature, dihydroxybenzoic acid levels in the striatum, and neuronal damage score were greater. The extent of lipid peroxidation in the brain and the rate of O2*- generation in the brain, liver, and heart were all greater in rats after heatstroke onset. In contrast, the values of total superoxide dismutase in the brain, liver, and heart and the catalase activity in the brain were lower. CONCLUSIONS: Taken together, these results indicate that hydroxyl radicals mediate cerebral ischemic injury associated with heatstroke.