Attenuation of reactive and active hyperemia by sympathetic stimulation in dog gracilis muscle.

The effects of sympathetic stimulation (SS) on reactive hyperemia (RH) and active hyperemia (AH) were evaluated in dog gracilis muscles. Sympathetic nerves to the muscle vasculature were activated by electrical stimulation of the obturator nerve during neuromuscular blockade. The frequency of stimulation was adjusted to decrease control conductance by 50%. RH responses to 1 and 5 min of arterial occlusion and AH after 1, 4, 7, and 10 s of tetanic contraction (direct muscle stimulation) at 30% maximal tensions were recorded in the absence and presence of SS. RH peak conductance (Cp), recovery half-time (T0.5), and excess flow (EQ) were significantly attenuated by SS at both occlusion durations. The change in conductance (delta C) during RH was not altered by SS, since the absolute reductions in control and peak conductances were not different. The Cp of AH was reduced at each contraction duration while the delta C was reduced only with 1-s contractions. The T0.5 and EQ of AH were not affected by SS. The data demonstrate that low frequency SS limits the degree of vasodilation associated with both muscle ischemia and tetanic contraction. Furthermore, the more pronounced effects of SS on RH suggest that there is greater inhibition of sympathetic vasoconstrictor influences associated with muscle contraction than muscle ischemia possibly due to the production of a substance during contraction, but not ischemia, that antagonizes sympathetic vasoconstrictor mechanisms.