Conditions for dipyridamole potentiation of skeletal muscle active hyperemia.

The effects of dipyridamole on active hyperemia were evaluated in dog gracilis muscles undergoing sustained isometric contractions. Muscles were stimulated to contract for 5, 15, 25, and 50 s at 20% maximal tension (20% Tmax) or for 10 s at 100% Tmax during intra-arterial infusion of either saline or dipyridamole (1 microM). In two separate groups of dogs, muscles were stimulated to contract under free-flow or restricted-flow (ischemic) conditions. In the later group, blood flow was reduced to 50% of precontraction level during the period of contraction. Dipyridamole increased resting vascular conductance by about 45%; however, it did not affect the change in vascular conductance resulting from muscle contraction. The recovery time for active hyperemia following free-flow contractions at 20% Tmax was not altered by dipyridamole. However, dipyridamole increased the recovery time following 50 s of restricted-flow contraction (20% Tmax) and 10 s of 100% Tmax contractions by 46 and 169%, respectively. These results suggest that adenosine contributes to active hyperemia following sustained ischemic contractions at 20% Tmax and contractions at 100% Tmax but not from contractions at 20% Tmax where blood flow is allowed to increase freely.