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Am J Physiol Heart Circ Physiol (May 16, 2002). doi:10.1152/ajpheart.00162.2002
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Articles in PresS, published online ahead of print May 16, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00162.2002
Submitted on February 27, 2002
Accepted on May 9, 2002

Mitochondrial respiratory control can compensate for intracellular O2 gradients in cardiomyocytes at low Po2

Eiji Takahashi1* and Koji Asano1

1 Physiology, Yamagata University School of Medicine, Yamagata, Japan

* To whom correspondence should be addressed. E-mail: eiji{at}med.id.yamagata-u.ac.jp.

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% O2, oxygen partial pressure (Po2) at the cell core dropped to 2.3 mmHg while 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% O2, radial oxygen gradients of similar magnitude were demonstrated (cell core Po2 = 2.6 mmHg). However, 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.




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