Effects Of An Acute Bout Of Strenuous Exercise On The Level Of NO/NOS In Rat's Myocardium Mitochondria, And Mitochondrial RCR, Ability Of Inhibition ROS And [Ca～(2+)]i

As cell's information molecular which have a lot of biological activity, NO has important regulated effect on cell mitochondria's physiological function, such as mitochondrial oxidative phosphorylation, the adjustment of cell's apoptosis, mitochondria DNA's metabolism and so on. The increasing of the producing NO can directly makes the function of the complex I, complex II and pyruvate dehydrogenase in the respiratory chain decreased. There is integrated L-Arg/NOS/NO producing system in the myocardium mitochondria. Today's research regards myocardium mitochondria as the main source of producing myocardium cell endogenous NO. Since NO is very important to mitochondrial respiration function and myocardium tissue is the exceptive tissue which mainly aerobic metabolize, the experiment is an acute bout of strenuous exercise model and observe in this exercise model's, the change of the ability between rats' myocardium cytosol and mitochondria NOS/NO, mitochondrial respiration control rate (RCR), the concentration of the free Ca²⁺ in mitochondria and the ability of mitochondrial inhibition to radical oxygen speices (O₂^-, OH ) so as to discuss NO's molecular mechanism to myocardium mitochondrial instantaneous adjustment in an acute bout of strenuous exercise situation.Put twelve 8-year-old female SD rats randomly divide into contrast group (six) and exercise group (six), all the mice engaged in three-day adaptable swimming, then let the rads of exercise group swim with heavy load for 20 min and rest for 2 min, later swam 299 ± 29 min averagely, then killed to get myocardium mitochondria to measure mitochondria RCR, total NOS, mtNOS activity of myocardium, the express level of myocardium III NOSmRNA, NO amount in myocardium cells and mitochondria, the ability of mitochondria's restrain to radical oxygen speices and [Ca²⁺]i. Results: ( l)Compare the total activity of rats' myocardium cells before with that after exercise, there is no significant difference in the statistics results (P = 0.054 > 0.05) ; the total activity of rats' myocardium mitochondria of exercise group is lower remarkably (P = 0.015<0.05) . (2)After exercise, eNOSmRNA express level of rats' myocardium cells didn't change a lot (P = 0.169>0.05); eNOSmRNA express level didn't change a lot either (P = 0.694>0.05) ; eNOSmRNA express level in exercise group is lower than contrast group remarkably (P =0.0280.05) . (3) Rats' myocardium mitochondrial inhibition ability to O₂ · dropped remarkably after exercise (P = 0.012<0.05) ; Rats' myocardium mitochondrial inhibition ability to ·HO dropped remarkably after exercise (P = 0.0120.05) . (1) After the exercise, the proportion of the mouse mitochondria respiration of state 3 and respiration of state 4 whose substrate was succinate didn't change with that before the exercise (P = 0.44 > 0.05) ; the proportion of the rats mitochondria respiration of state 3 and respiration of state 4 whose substrate was malate didn't change either (P = 0.964 >0.05 ) . (5) After the exercise, Rats' myocardium mitochondria [Ca2+]i didn't change a lot (P = 0.1>0.05) . Conclusion: (1) after acute and long-term swimming, the express level of rats' myocardium cell cNOSmRNA was not changed, the express level of iNOSmRNA decreased remarkably, total NOS activity of myocardium cell had some descend, mtNOS activity decreased remarkably, which is probably the direct reason for the obvious descend of myocardium cells and mitochondria NO. (2) After the exercise, the ability of rats' mitochondrial restrain to Reactive Oxygen Species (O2"'-. OH ') decreased. But after the exercise, rats' myocardium mitochondrial respiration controlling rate didn't change no matter with succinate or malate as reaction substrate. The concentration of mitochondria free Ca2+ has the trend of decreasing, but not remarkable, which shows in this exercise model, the function of myocardium mitochondria can keep normal to fit for oxidative stress of exercise. (3) Because of the down regulation of the level of mitochondrial NO after exercise, NO can't be combined with O...