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Department of Physiology, University of Leeds.

1. In dogs anaesthetized with sodium pentobarbitone and artificially ventilated, the gracilis muscles were vascularly isolated and perfused at a constant flow rate of 51.2 +/- 9.8 ml min-1 100 g-1 muscle tissue (183 +/- 17.8% of resting blood flow; mean +/- S.E.; n = 13). 2. Electrical stimulation of the cut peripheral end of the obturator nerve (6 V, 4 Hz) resulted in muscle contraction (658 +/- 118 g 100 g-1 force after 5 min), and an immediate decrease in arterial perfusion pressure from 179 +/- 15.7 mmHg to 87 +/- 10.0 mmHg (51.4 +/- 4.5% decrease in vascular resistance after 2 min of contraction). Venous oxygen tension decreased from 69.2 +/- 5.1 mmHg to 18.5 +/- 1.4 mmHg (n = 6). These values did not significantly alter during the remaining period of stimulation (10-20 min). 3. The concentration of adenosine in arterial plasma did not change significantly during muscle contraction (137 +/- 23 nM; n = 10). However, the adenosine concentrations in venous plasma showed a significant (P less than 0.01) increase from a control value of 164 +/- 55 nM to 455 +/- 77 nM (n = 9) after 5 min of muscle contraction and remained high during the rest of the 20 min contraction. In six of the dogs adenosine concentrations were determined after 1 and 3 min of contraction and showed a smaller but statistically significant (P less than 0.05) rise in venous concentration. 4. During infusion of adenosine into the artery to give plasma concentrations between 0.3 microM and 1 mM, 72.6 +/- 2.1% (n = 29) of the infused adenosine was taken up by the tissues before it reached the vein. Comparison of vasodilatation and venous adenosine concentrations during adenosine infusion and muscle contractions showed that the released adenosine could contribute about 15% to the total vasodilatation after 1 min and about 40% between 5 and 20 min of contractions. Released adenosine could contribute about 80% to the vasodilatation that remained 5 min after the withdrawal of stimulation. Arterial perfusion pressure took 22 min to return to control, whereas adenosine release had fallen to zero within 10 min. 5. These data suggest that the released adenosine could contribute to exercise hyperaemia, but is unlikely to be the main factor, particularly in the initial stage.

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