Reduction of contraction-induced arteriolar vasodilation by adenosine deaminase or theophylline.

To test the hypothesis that adenosine mediates striated muscle blood flow, the cremaster muscle microcirculation was exposed to a continuous superfusion (10-30 min) of either a control, adenosine deaminase (7 micrograms protein/ml), or theophylline (10(-5) M) solution before, during, and following twitch contraction. Small arteriolar diameter and (dual-slit) blood flow velocity were continuously measured for 3 min before and after 2 min of electrical stimulation at 10, 5, or 2 Hz. Estimated arteriolar volume flow was calculated at 10-s intervals. The peak and average arteriolar diameter, peak and average estimated volume flow, duration of the exercise evoked response, and the total estimated volume of blood delivered in the 3-min postexercise period were reduced by deaminase as a function of stimulus frequency relative to a paired control. Deaminase reduced total estimated blood flow by 44, 35, and 22% at 10, 5, and 2 Hz, respectively. Although theophylline was more damaging to the tissue at a dose that was equieffective with deaminase, it produced a consistent reduction in peak and average arteriolar diameter and estimated volume flow after 5-Hz exercise. If changes in small arteriolar diameter are proportional to tissue blood flow changes, then these observations support the hypothesis that adenosine contributes to contraction-induced hyperemia in skeletal muscle in free-flow conditions and that its regulatory contribution depends on the intensity of the metabolic stimulus. Alternatively, these data could implicate adenosine in exercise-induced capillary recruitment.