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Jeffrey L Jasperse

Publications and source records attributed to Jeffrey L Jasperse.

2 recordsLinked to original sources
PubMed2006

Mechanical compression elicits vasodilatation in rat skeletal muscle feed arteries.

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.

Animals↗
PubMed2006

Endothelial function and exercise training: evidence from studies using animal models.

This review summarizes and examines the evidence from experiments using animal models to determine the effect of endurance exercise training on endothelium-dependent dilation in the arterial circulation. The response of the endothelium to exercise training is complex and depends on a number of factors that include the duration of the training program, the size of the artery/arteriole, the anatomical location of the artery/arteriole, and the health of the individual. In healthy animals, short-term exercise training appears to cause enhanced endothelium-dependent dilation in some vascular beds, but it returns to normal levels as the duration of the training program increases. In general, evidence supports the notion that exercise training causes greater increases in endothelium-dependent dilation in various disease states than in healthy individuals. The evidence of a generalized effect of training on arterial endothelium in all regions of the body is inconsistent and appears to depend on the animal model used. Available results indicate that training duration, artery size, and anatomical location interact in ways not fully understood at this time to determine whether and to what extent endothelium-dependent dilation will be enhanced by exercise training.

Animals↗