The changes of mitochondrial functions of myocardium in heat-stressed rats
Qian Ling
Abstract
Qian Ling
Abstract
AIM:To study the changes of mitochondrial oxidative phosphorylation and calcium metabolism of myocardium in heat-stressed rats METHODS:The mitochondrial oxidative metabolism was analysed by Klark oxygen-electrode polarography; Bioluminescence assay was used to measure ATP content in myocardium and Ca 2+ -ATPase activity of mitochondria; calcium content in mitochondria was measured by ICP RESULTS:The respiratory control rate (RCR) and P/O ratio decreased gradually as rectal temperature (Tr) increased When Tr rosed to 42℃, RCR and P/O ratio decreased by 31 4% and 11 05% ( P 0 05) respectively RCR decrease resulted mainly from the effect of respiratory state Ⅳ ATP content in myocardium of heat-stressed rats also decreased by 37 5% at Tr42℃ The activity of Ca 2+ -ATPase and calcium content in myocardial mitochondria of heat-stressed rats were reduced When Tr increased to 42℃, both of the above decreased by 32 6% and 31 3% respectively compared with control group CONCLUSION:The injury of oxidative respiration and Ca 2+ -metabolism of mitochondria may be one important cause resulting in cardiac-function disorder in heat stress
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AIM:To study the changes of mitochondrial oxidative phosphorylation and calcium metabolism of myocardium in heat-stressed rats METHODS:The mitochondrial oxidative metabolism was analysed by Klark oxygen-electrode polarography; Bioluminescence assay was used to measure ATP content in myocardium and Ca 2+ -ATPase activity of mitochondria; calcium content in mitochondria was measured by ICP RESULTS:The respiratory control rate (RCR) and P/O ratio decreased gradually as rectal temperature (Tr) increased When Tr rosed to 42℃, RCR and P/O ratio decreased by 31 4% and 11 05% ( P 0 05) respectively RCR decrease resulted mainly from the effect of respiratory state Ⅳ ATP content in myocardium of heat-stressed rats also decreased by 37 5% at Tr42℃ The activity of Ca 2+ -ATPase and calcium content in myocardial mitochondria of heat-stressed rats were reduced When Tr increased to 42℃, both of the above decreased by 32 6% and 31 3% respectively compared with control group CONCLUSION:The injury of oxidative respiration and Ca 2+ -metabolism of mitochondria may be one important cause resulting in cardiac-function disorder in heat stress
Key concepts: Mitochondrion, Oxidative phosphorylation, Calcium, Internal medicine, Respiration, Chemistry, Endocrinology, ATPase