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Vol. 84, Issue 2, 754-758, February 1998
Department of Anesthesiology, Mayo Clinic and Foundation, Rochester, Minnesota 55905; and Department of Internal Medicine, University of Texas Southwestern Medical School, Dallas, Texas 75235
Dyke, Christopher K., Niki M. Dietz, Robert L. Lennon, David
O. Warner, and Michael J. Joyner. Forearm blood flow responses to
handgripping after local neuromuscular blockade. J. Appl. Physiol. 84(2): 754-758, 1998.
To test the
hypothesis that acetylcholine "spillover" from motor nerves
contributes significantly to skeletal muscle vasodilation during
exercise, we measured the forearm blood flow responses during attempted
handgripping after local paralysis of the forearm with the
neuromuscular-blocking drug pipecuronium. This compound blocks
postsynaptic nicotinic receptors but has no impact on acetylcholine
release from motor nerves. The drug was administered selectively to one
forearm by using regional intravenous drug administration techniques in
five subjects. Pipecuronium reduced maximum forearm grip strength from
40.0 ± 3.2 kg before treatment to 0.0 kg after treatment. By
contrast, drug administration had no effect on maximum voluntary
contraction in the untreated forearm (41.3 ± 3.3 vs. 41.4 ± 2.7 kg). During 2 min of attempted maximal contraction of the paralyzed
forearm, the forearm blood flow increased from only 3.4 ± 0.8 to
4.8 ± 1.2 ml · 100 ml
1 · min
1
(P < 0.05). Heart rate increased
from 63 ± 3 to 73 ± 8 beats/min (P > 0.05) during attempted
contraction, and only three of five subjects showed obvious increases
in heart rate. Mean arterial pressure increased significantly
(P < 0.05) from 102 ± 6 to 109 ± 9 mmHg during attempted contractions. When these increases in flow are considered in the context of the marked (10-fold or greater) increases in flow seen in contracting forearm skeletal muscle, it
appears that acetylcholine spillover from motor nerves has, at most, a
minimal impact on the hyperemic responses to contraction in humans.
muscle blood flow; exercise hyperemia; active vasodilation
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