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Protective effects of α‐tocopherol and mannitol in both circulatory shock and cerebral ischaemia injury in rat heatstroke
Author(s) -
Niu KC,
Lin KC,
Yang CY,
Lin MT
Publication year - 2003
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2003.03905.x
Subject(s) - heatstroke , lipid peroxidation , anesthesia , medicine , stroke (engine) , mannitol , ischemia , alpha tocopherol , chemistry , heat shock protein , oxidative stress , shock (circulatory) , brain damage , vitamin e , endocrinology , antioxidant , biochemistry , mechanical engineering , engineering , gene
Summary 1. There is evidence that hydroxyl radicals are accumulated and oxidative stress is produced in multiple organs, including the brain, of rats with heat stroke. Herein, we investigated the effect on heat stroke‐induced circulatory shock and cerebral ischaemic injury of two free radical scavengers, namely mannitol and α‐tocopherol. 2. Urethane‐anaesthetized rats were exposed to heat stress (ambient temperature 42°C) to induce heat stroke. Control rats were exposed to 24°C. Mean arterial pressure and cerebral blood flow after the onset of heat stroke were significantly lower in heat stroke rats than in control rats. However, cerebral free radicals, lipid peroxidation and the neuronal damage score were greater in heat stroke rats compared with control rats. Similarly, plasma cytokines, including tumour necrosis factor‐α, interleukin (IL)‐1β and IL‐6, were significantly higher in heat stroke rats compared with their normothermic controls. 3. Pretreatment with α‐tocopherol (20 mg/kg, i.v.) or mannitol (10%, i.v.) 30 min before the onset of heat exposure significantly attenuated heat stroke‐induced arterial hypotension, cerebral ischaemia and neuronal damage, the increased free radical formation and lipid peroxidation in the brain and the increased plasma levels of cytokines. Pretreatment with α‐tocopherol or mannitol resulted in a prolongation of survival time in heat stroke. 4. These results demonstrate that although pretreatment with α‐tocopherol and mannitol does not prevent the heat stroke syndrome entirely, an attenuation of the syndrome is observed.