Rapid vasodilation in response to a brief tetanic muscle contraction

To test the hypothesis that vasodilation occurs because of the release of a vasoactive substance after a brief muscle contraction and to determine whe ther acetylcholine spillover from the motor nerve is involved in contractio n-induced hyperemia, tetanic muscle contractions were produced by sciatic n erve stimulation in anesthetized dogs (n = 16), instrumented with flow prob es on both external iliac arteries. A 1-s stimulation of the sciatic nerve at 1.5, 3, and 10 times motor threshold increased blood flow above baseline (P < 0.01) for 20, 25, and 30 s, respectively. Blood flow was significantl y greater 1 s after the contraction ended for 3 and 10 x motor threshold (P < 0.01) and did not peak until 6-7 s after the contraction. The elevations in blood flow to a 1-s stimulation of the sciatic nerve and a 30-s train o f stimulations were abolished by neuromuscular blockade (vecuronium). The d elayed peak blood flow response and the prolonged hyperemia suggest that a vasoactive substance is rapidly released from the contracting skeletal musc le and can affect blood flow with removal of the mechanical constraint impo sed by the contraction. In addition, acetylcholine spill-over from the moto r nerve is not responsible for the increase in blood flow in response to mu scle contraction.