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Department of Physiology, University of Arizona Health Sciences Center, Tucson, Arizona 85724
The main purpose of this study was to determine the interstitial oxygen tension at which aerobic metabolism becomes limited (critical PO2) in vivo in resting skeletal muscle. Using an intravital microscope system, we determined the interstitial oxygen tension at 20-µm-diameter tissue sites in rat spinotrapezius muscle from the phosphorescence lifetime decay of a metalloporphyrin probe during a 1-min stoppage of muscle blood flow. In paired experiments NADH fluorescence was measured at the same sites during flow stoppage. NADH fluorescence rose significantly above control when interstitial PO2 fell to 2.9 ± 0.5 mmHg (n = 13) and was not significantly different (2.4 ± 0.5 mmHg) when the two variables were first averaged for all sites and then compared. Similar values were obtained using the abrupt change in rate of PO2 decline as the criterion for critical PO2. With a similar protocol, we determined that NADH rose significantly at a tissue site centered 30 µm from a collecting venule when intravascular PO2 fell to 7.2 ± 1.5 mmHg. The values for critical interstitial and critical intravascular PO2 are well below those reported during free blood flow in this and in other muscle preparations, suggesting that oxygen delivery is regulated at levels well above the minimum required for oxidative metabolism. The extracellular critical PO2 found in this study is slightly greater than previously found in vitro, possibly due to differing local conditions rather than a difference in metabolic set point for the mitochondria.
metabolic hypothesis; reduced nicotinamide adenine dinucleotide; oxidative metabolism; oxygen delivery; in vivo microscopy; phosphorescence lifetime
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