Effect of vecuronium on the release of acetylcholine after nerve stimulation

To test the hypothesis that vasodilation occurs because of the release of a vasoactive substance after a brief muscle contraction and to determine whether acetylcholine spillover from the motor nerve is involved in contraction-induced hyperemia, tetanic muscle contractions were produced by sciatic nerve stimulation in anesthetized dogs (n = 16), instrumented with flow probes 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 significantly greater I 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 of stimulations were abolished by neuromuscular blockade (vecuronium b). The delayed peak blood flow response and the prolonged hyperemia suggest that a vasoactive substance is rapidly released from the contracting skeletal muscle and can affect blood flow with removal of the mechanical constraint imposed by the contraction. In addition, acetylcholine spill-over from the motor nerve is not responsible for the increase in blood flow in response to muscle contraction.