论文部分内容阅读
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。
Objective: To observe the changes of mitochondrial oxidative phosphorylation and calcium storage in heat-stressed rats. Methods: The mitochondrial oxidative metabolism was measured by Klark oxygen polarographic method. The content of ATP and mitochondrial Ca2 + -ATPase in ventricular myocardium were measured by bioluminescence method. The content of calcium in myocardial mitochondria was measured by inductively coupled plasma atomic emission spectrometry. Results: The mitochondrial respiratory control (RCR) and oxidative phosphorylation (P / O) of heat-stressed rats decreased gradually and gradually with the rectal temperature increasing. When the rectal temperature of rats was higher than 42 ℃, RCR Compared with the control, P / O decreased by 314% and 1105% respectively. Rectal temperature above 42 ℃, ATP content in rat ventricular muscle was only 37.5% of the control. The mitochondrial Ca2 + -ATPase activity and calcium content were also significantly decreased in the heat-stressed rat myocardium. The two indexes of rectal temperature above 42 ℃ were reduced by 32.6% and 313% compared with the control group, respectively. Abnormal changes in calcium metabolism. Conclusion: The oxidative metabolism and impaired calcium function of myocardial mitochondria in heat stress are the important causes of cardiac dysfunction during heat stress.