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首页> 外文期刊>American Journal of Physiology >Implication of CO inactivation on myoglobin function.
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Implication of CO inactivation on myoglobin function.

机译：CO失活对肌红蛋白功能的影响。

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Myoglobin (Mb) has a purported role in facilitating O2 diffusion in tissue, especially as cellular PO2 drops or the respiration demand increases. Inhibiting Mb with CO under conditions that accentuate the facilitated diffusion role should then elicit a significant physiological response. In one set of experiments, the perfused myocardium received buffer with decreasing PO2 (225, 129, and 64 mmHg). Intracellular PO2 declined, as reflected in the 1H NMR Val E11 signal of MbO2 (67%, 32%, and 18%). The addition of 6% CO further reduced the available MbO2 (11%, 9%, and 7%), as evidenced by the decline of the MbO2 Val E11 signal intensity at -2.76 ppm. In a second set of experiments, electrical stimulation increased the heart rate (300, 450, and 540 beats/min) and correspondingly the O2 consumption rate (MVO2). Intracellular PO2 also declined, as reflected in the slight drop in the MbO2 signal (100%, 96%, and 82%). MVO2 increased (100%, 114%, 165%). The addition of 3% CO in the stimulated hearts further decreased the available MbO2 (46%, 44%, and 29%). In all cases, CO inactivation of Mb does not induce any change in the respiration rate, contractile function, and high-energy phosphate levels. Moreover, the MbCO/MbO2 partition coefficient shifts dramatically from its in vitro value during hypoxia and increased work. The observation suggests a modulation of an intracellular O2 gradient. Overall, the experimental observations provide no evidence of a facilitated diffusion role for Mb in perfused myocardium and implicate a physiologically responsive intracellular O2 gradient.
机译：据说肌红蛋白（Mb）在促进O2在组织中扩散方面起着重要的作用，特别是当细胞PO2下降或呼吸需求增加时。然后，在强调促进扩散作用的条件下用CO抑制Mb应当引起明显的生理反应。在一组实验中，灌注的心肌所接受的缓冲液的PO2降低（225、129和64 mmHg）。 MbO2的1H NMR Val E11信号反映出细胞内PO2下降（67％，32％和18％）。添加6％的CO进一步减少了可用的MbO2（11％，9％和7％），如MbO2 Val E11信号强度在-2.76 ppm处下降所证明。在第二组实验中，电刺激提高了心率（300、450和540次/分钟），并相应提高了O2消耗率（MVO2）。 MbO2信号略有下降（100％，96％和82％）也反映出细胞内PO2下降。 MVO2增加（100％，114％，165％）。在受刺激的心脏中添加3％的CO进一步降低了可用的MbO2（46％，44％和29％）。在所有情况下，CO灭活Mb都不会引起呼吸频率，收缩功能和高能磷酸盐水平的任何变化。此外，在缺氧和增加功的过程中，MbCO / MbO2分配系数从其体外值显着变化。该发现表明细胞内O 2梯度的调节。总体而言，实验观察结果没有提供Mb在灌注心肌中促进扩散作用的证据，并且暗示了生理反应性细胞内O2梯度。

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