Observations on the Role of Diminished Oxygen Tension in the Functional Hyperemia of Skeletal Muscle
The hypothesis that lowered tissue oxygen tension acting on vascular smooth muscle can explain functional hyperemia in skeletal muscle was examined in ten dogs. A comparison was made between the blood flow increment that accompanied rapid, rhythmic contraction of a gastrocnemius muscle and the flow change that occurred in the same muscle at rest during its perfusion with venous blood obtained from the resting or contracting gastrocnemius muscle of the opposite leg. Blood POO2, pH, and PCOCO2 were measured in samples of venous blood from the muscle. There was no evidence that the perfusion circuit traumatized the perfused blood. During functional hyperemia, the increases in blood flow averaged 173%, and the average venous POO2, was 25 mm Hg. During venous perfusion, the maximum increases in blood flow averaged 56%, and the average venous POO2, was 23 mm Hg. When the muscle was stimulated to contract during its perfusion with venous blood, increases in blood flow occurred which averaged 143%, despite additional falls in venous blood POO2 that averaged only 3 mm Hg. These studies suggest that the effect of lowered POO2 on vascular smooth muscle does not produce sufficient vasodilatation to explain functional hyperemia in skeletal muscle.
- Received May 18, 1964.
- © 1964 American Heart Association, Inc.