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Am J Physiol Heart Circ Physiol 283: H871-H878, 2002. First published May 16, 2002; doi:10.1152/ajpheart.00162.2002
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Vol. 283, Issue 3, H871-H878, September 2002

Mitochondrial respiratory control can compensate for intracellular O2 gradients in cardiomyocytes at low PO2

Eiji Takahashi and Koji Asano

Department of Physiology, Yamagata University School of Medicine, Yamagata 990-9585, Japan

In isolated single cardiomyocytes with moderately elevated mitochondrial respiration, direct evidence for intracellular radial gradients of oxygen concentration was obtained by subcellular spectrophotometry of myoglobin (Mb). When oxygen consumption was increased by carbonyl cyanide m-chlorophenylhydrazone (CCCP) during superfusion of cells with 4% oxygen, PO2 at the cell core dropped to 2.3 mmHg, whereas Mb near the plasma membrane was almost fully saturated with oxygen. Subcellular NADH fluorometry demonstrated corresponding intracellular heterogeneities of NADH, indicating suppression of mitochondrial oxidative metabolism due to relatively slow intracellular oxygen diffusion. When oxygen consumption was increased by electrical pacing in 2% oxygen, radial oxygen gradients of similar magnitude were demonstrated (cell core PO2 = 2.6 mmHg). However, an increase in NADH fluorescence at the cell core was not detected. Because CCCP abolished mitochondrial respiratory control while it was intact in electrically paced cardiomyocytes, we conclude that mitochondria with intact respiratory control can sustain electron transfer with reduced oxygen supply. Thus mitochondrial intrinsic regulation can compensate for relatively slow oxygen diffusion within cardiomyocytes.

spectrophotometry; myoglobin; radial oxygen gradients; NADH


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