摘要
目的：观察不同强度热应激大鼠心肌线粒体氧化磷酸化功能和钙储存功能的变化。方法：用Ｋｌａｒｋ氧电极极谱方法测定线粒体氧化代谢功能，用生物发光法测定心室肌ＡＴＰ含量及线粒体Ｃａ２＋－ＡＴＰ酶活性，用电感藕合等离子体－原子放射光谱仪测定心肌线粒体内钙含量。结果：热应激大鼠心肌线粒体呼吸控制率（ｒｅｓｐｉｒａｔｏｒｙｃｏｎｔｒｏｌｒａｔｉｏ，ＲＣＲ）及氧化磷酸化效率（Ｐ／Ｏ）均随动物直肠温度的升高逐步显著降低，当大鼠直肠温度超过４２℃时，ＲＣＲ与Ｐ／Ｏ分别较对照下降３１４％，１１０５％。直肠温度４２℃以上，大鼠的心室肌ＡＴＰ含量仅为对照的３７５％。热应激大鼠心肌线粒体Ｃａ２＋－ＡＴＰ酶活性和钙含量亦明显降低，直肠温度４２℃以上大鼠的该两项指标可较对照值降低达３２６％和３１３％，显示了线粒体钙代谢的异常变化。结论：热应激机体心肌线粒体的氧化代谢和钙功能受损是热应激时心功能紊乱的重要原因。
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 Tr>42℃ 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
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第4期333-335,共3页
Chinese Journal of Pathophysiology
关键词
线粒体
钙代谢障碍
热应激
心血管
大鼠
MeSH Heat
Stress
Mitochondria, heart
Oxidative phosphorylation
Calcium metabolism disorders
