BACKGROUND: Although brain cooling has recently been reported as effective in improving the survival after heatstroke generation in rats, the mechanisms underlying the therapeutic effects of brain cooling are not fully elucidated. This study was conducted to test whether the acute lung inflammation and damage that might occur during heatstroke could be affected by brain cooling. METHODS: Anesthetized rats were randomized into four groups as follows: (a) normothermic controls (n = 8); (b) heatstroke rats without saline delivery (n = 8); (c) heatstroke rats treated with 36°C saline via retrograde jugular vein (n = 8); and (d) heatstroke rats treated with 4°C saline via retrograde jugular vein (n = 8). Heatstroke was induced by putting the animals in a folded heating pad of 42°C for 68 minutes controlled by circulating hot water. The core temperatures of normothermic groups were maintained at about 36°C. The cardiovascular parameters and core temperatures were monitored for all experiments. Bronchoalveolar lavage (BAL) was done in the left lung 20 minutes after termination of heat stress for determination of cellular ischemia markers (e.g., glutamate, lactate-to-pyruvate ratio), proinflammatory cytokines (interleukin-1, tumor necrosis factor-alpha), and nitric oxide metabolites. Parts of the right lung were excised for meloperoxidase measurement, whereas the rest was collected for lung damage score assessments. RESULTS: When compared with those of normothermic controls, untreated or 36°C saline-treated heatstroke rats had higher values of BAL fluid levels of cellular ischemia markers, proinflammatory cytokines, nitric oxide metabolites, lung meroperoxidase activity, lung damage score, and neutrophil infiltration. Brain cooling causes by 4°C saline infusion significantly reduced the heat-induced increased BAL levels of cellular ischemia markers, proinflammatory cytokines, and nitric oxide metabolites, and reduced lung damage score and neutrophil infiltration. CONCLUSIONS: These experimental data indicate that acute lung inflammation and damage is a target of brain cooling after heatstroke injury.
BACKGROUND: Although brain cooling has recently been reported as effective in improving the survival after heatstroke generation in rats, the mechanisms underlying the therapeutic effects of brain cooling are not fully elucidated. This study was conducted to test whether the acute lung inflammation and damage that might occur during heatstroke could be affected by brain cooling. METHODS: Anesthetized rats were randomized into four groups as follows: (a) normothermic controls (n = 8); (b) heatstrokerats without saline delivery (n = 8); (c) heatstrokerats treated with 36°C saline via retrograde jugular vein (n = 8); and (d) heatstrokerats treated with 4°C saline via retrograde jugular vein (n = 8). Heatstroke was induced by putting the animals in a folded heating pad of 42°C for 68 minutes controlled by circulating hot water. The core temperatures of normothermic groups were maintained at about 36°C. The cardiovascular parameters and core temperatures were monitored for all experiments. Bronchoalveolar lavage (BAL) was done in the left lung 20 minutes after termination of heat stress for determination of cellular ischemia markers (e.g., glutamate, lactate-to-pyruvate ratio), proinflammatory cytokines (interleukin-1, tumor necrosis factor-alpha), and nitric oxide metabolites. Parts of the right lung were excised for meloperoxidase measurement, whereas the rest was collected for lung damage score assessments. RESULTS: When compared with those of normothermic controls, untreated or 36°C saline-treated heatstrokerats had higher values of BAL fluid levels of cellular ischemia markers, proinflammatory cytokines, nitric oxide metabolites, lung meroperoxidase activity, lung damage score, and neutrophil infiltration. Brain cooling causes by 4°C saline infusion significantly reduced the heat-induced increased BAL levels of cellular ischemia markers, proinflammatory cytokines, and nitric oxide metabolites, and reduced lung damage score and neutrophil infiltration. CONCLUSIONS: These experimental data indicate that acute lung inflammation and damage is a target of brain cooling after heatstroke injury.