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. 2006 Apr 15;572(Pt 2):561-7.
doi: 10.1113/jphysiol.2005.099507. Epub 2006 Feb 23.

Mechanical compression elicits vasodilatation in rat skeletal muscle feed arteries

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Mechanical compression elicits vasodilatation in rat skeletal muscle feed arteries

Philip S Clifford et al. J Physiol. .

Abstract

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.

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Figures

Figure 1
Figure 1. Response of a single soleus feed artery to external pressure
1 × 1 signifies one pressure pulse of 1 s duration; 1 × 5 signifies one pressure pulse of 5 s duration; and 5 × 1 signifies five separate 1 s pulses with 1 s between each pulse. Diameters were tracked manually by moving a cursor on the video screen.
Figure 2
Figure 2. Dilatation produced by compression of soleus feed arteries in series 1 (n = 6)
1 × 1 signifies one pressure pulse of 1 s duration; 1 × 5 signifies one pressure pulse of 5 s duration; and 5 × 1 signifies five separate 1 s pulses with 1 s between each pulse. *P < 0.01 compared to 1 × 1 and 1 × 5.
Figure 3
Figure 3. Dilatation produced by compression of intact and endothelium-denuded soleus feed arteries in series 2 (n = 9)
1 × 1 signifies one pressure pulse of 1 s duration; 1 × 5 signifies one pressure pulse of 5 s duration; and 5 × 1 signifies five separate 1 s pulses with 1 s between each pulse. *P < 0.01 compared to 1 × 1 and 1 × 5; †P < 0.01 compared to intact condition.

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