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Am J Physiol Heart Circ Physiol (May 23, 2002). doi:10.1152/ajpheart.00050.2002
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Articles in PresS, published online ahead of print May 23, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00050.2002
Submitted on January 22, 2002
Accepted on May 13, 2002

EFFECT OF CARDIAC PACING ON FOREARM VASCULAR RESPONSES AND NITRIC OXIDE FUNCTION

Daniel J. Green1*, Craig Cheetham1, Chelsea Henderson2, Ruckshen Weerasooriya3, and Gerry O'Driscoll4

1 Human Movement and Exercise Science, The University of Western Australia, Crawley, WA, Australia; Cardiac Transplant Unit, Royal Perth Hospital, Perth, WA, Australia; Cardiology, Royal Perth Hopsital, Perth, WA, Australia
2 Human Movement and Exercise Science, The University of Western Australia, Crawley, WA, Australia
3 Cardiology, Royal Perth Hopsital, Perth, WA, Australia
4 Cardiac Transplant Unit, Royal Perth Hospital, Perth, WA, Australia; Cardiology, Royal Perth Hopsital, Perth, WA, Australia; Human Movement and Exercise Science, The University of Western Australia, Crawley, WA, Australia

* To whom correspondence should be addressed. E-mail: brevis{at}cyllene.uwa.edu.au.

We examined the hypothesis that changes in heart rate at rest influence bioactivity of nitric oxide (NO) in humans, by examining forearm blood flow responses during cardiac pacing in six subjects. Peak forearm blood flow (PFBF) and mean blood flow across the cardiac cycle (MFBF) were continuously recorded at baseline and during pacing, using high resolution brachial artery ultrasound and Doppler flow velocity (v) measurement. The brachial artery was cannulated to allow continuous infusion of saline or L-NMMA. As heart rate increased, no changes in pulse pressure, mean or peak blood flow were evident. L-NMMA had no effect on brachial artery diameter, velocity or flows when compared to saline infusion. These results contrast with our recent findings that exercise involving the lower body, associated with increases in heart rate and pulse pressure, also increased forearm blood flows, the latter responses being diminished by L-NMMA. These data suggest that changes in blood pressure, rather than pulse frequency, may be the stimulus for shear stress-mediated NO release in vivo.




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