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J Physiol Volume 572, Number 2, 561-567, April 15, 2006 DOI: 10.1113/jphysiol.2005.099507
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Skeletal Muscle and Exercise

Mechanical compression elicits vasodilatation in rat skeletal muscle feed arteries

Philip S. Clifford1, Heidi A. Kluess1, Jason J. Hamann1, John B. Buckwalter1 and Jeffrey L. Jasperse2

1 Medical College of Wisconsin and VA Medical Center, Milwaukee, WI 53295, USA
2 Pepperdine University, Malibu, CA 90263, USA

To date, no satisfactory explanation has been provided for the immediate increase in blood flow to skeletal muscles at the onset of exercise. We hypothesized that rapid vasodilatation is a consequence of release of a vasoactive substance from the endothelium owing to mechanical deformation of the vasculature during contraction. Rat soleus feed arteries were isolated, removed and mounted on micropipettes in a sealed chamber. Arteries were pressurized to 68 mmHg, and luminal diameter was measured using an inverted microscope. Pressure pulses of 600 mmHg were delivered for 1 s, 5 s, and as a series of five repeated 1 s pulses with 1 s between pulses. During application of external pressure the lumen of the artery was completely closed, but immediately following release of pressure the diameter was significantly increased. In intact arteries (series 1, n= 6) for the 1 s pulse, 5 s pulse and series of five 1 s pulses, the peak increases in diameter were, respectively, (mean ±S.E.M.) 16 ± 2, 14 ± 2 and 27 ± 3%, with respective times from release of pressure to peak diameter of 4.1 ± 0.3, 4.6 ± 0.7 and 2.8 ± 0.4 s. In series 2 (n= 9) the arteries increased diameter by 15 ± 2, 15 ± 2 and 30 ± 3% before and by 8 ± 1, 8 ± 1 and 21 ± 2% after removal of the endothelium with air. The important new finding in these experiments is that mechanical compression caused dilatation of skeletal muscle feed arteries with a time course similar to the change in blood flow after a brief muscle contraction. The magnitude of dilatation was not affected by increasing the duration of compression but was enhanced by increasing the number of compressions. Since removal of the endothelium reduced but did not abolish the dilatation in response to mechanical compression, it appears that the dilatation is mediated by both endothelium-dependent and -independent signalling pathways.

(Received 3 October 2005; accepted after revision 20 February 2006; first published online 23 February 2006)
Corresponding author P. S. Clifford: Anesthesia Research 151, VA Medical Center, 5000 W National Ave., Milwaukee, WI 53295, USA. Email: pcliff{at}mcw.edu




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