Arai A E, Kasserra C E, Territo P R, Gandjbakhche A H, Balaban R S
Laboratory of Cardiac Energetics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Am J Physiol. 1999 Aug;277(2):H683-97. doi: 10.1152/ajpheart.1999.277.2.H683.
The oxygenation state of myoglobin and the redox state of cytochrome c provide information on the PO(2) in the cytosol and mitochondria, respectively. An optical "window" from approximately 540 to 585 nm was found in the pig heart in vivo that permitted the monitoring of myoglobin and cytochrome c without interference from Hb oxygenation or blood volume. Scanning reflectance spectroscopy was performed on the surgically exposed left ventricle of pigs. Difference spectra between control and a total left anterior descending coronary artery occlusion revealed maxima and minima in this spectral region consistent with myoglobin deoxygenation and cytochrome c and b reduction. Comparison of in vivo data with in vitro fractions of the heart, including Hb-free tissue whole heart and homogenates, mitochondria, myoglobin, and pig red blood cells, reveals minimal contributions of Hb in vivo. This conclusion was confirmed by expanding the blood volume of the myocardium and increasing mean Hb O(2) saturation with an intracoronary infusion of adenosine (20 microgram. kg(-1). min(-1)), which had no significant effect on the 540- to 585-nm region. These results also suggested that myoglobin O(2) saturation was not blood flow limited under these conditions in vivo. Work jump studies with phenylephrine also failed to change cytochrome c redox state or myoglobin oxygenation. Computer simulations using recent physical data are consistent with the notion that myoglobin O(2) saturation is >92% under basal conditions and does not change significantly with moderate workloads. These studies show that reflectance spectroscopy can assess myocardial oxygenation in vivo. Myoglobin O(2) saturation is very high and is not labile to moderate changes in cardiac workload in the open-chest pig model. These findings indicate that myoglobin does not contribute significantly to O(2) transport via facilitated diffusion under these conditions.
肌红蛋白的氧合状态和细胞色素c的氧化还原状态分别提供了关于细胞质和线粒体中氧分压（PO₂）的信息。在猪心脏活体中发现了一个约540至585nm的光学“窗口”，可在此窗口监测肌红蛋白和细胞色素c，而不受血红蛋白氧合或血容量的干扰。对猪手术暴露的左心室进行扫描反射光谱分析。对照与左前降支冠状动脉完全闭塞之间的差异光谱显示，该光谱区域的最大值和最小值与肌红蛋白脱氧以及细胞色素c和b的还原一致。将活体数据与心脏的体外组分进行比较，包括无血红蛋白组织全心脏和匀浆、线粒体、肌红蛋白以及猪红细胞，结果显示血红蛋白在活体中的贡献极小。通过冠状动脉内输注腺苷（20μg·kg⁻¹·min⁻¹）来增加心肌血容量并提高平均血红蛋白氧饱和度，这对540至585nm区域没有显著影响，从而证实了这一结论。这些结果还表明，在这些活体条件下，肌红蛋白的氧饱和度不受血流限制。使用去氧肾上腺素进行的功跃变研究也未能改变细胞色素c的氧化还原状态或肌红蛋白的氧合情况。利用最新物理数据进行的计算机模拟与以下观点一致：在基础条件下，肌红蛋白的氧饱和度>92%，并且在适度工作负荷下不会发生显著变化。这些研究表明，反射光谱可用于评估活体心肌的氧合情况。在开胸猪模型中，肌红蛋白的氧饱和度非常高，并且对心脏工作负荷的适度变化不敏感。这些发现表明，在这些条件下，肌红蛋白通过易化扩散对氧运输的贡献不大。
