Role of arterial PO2 and PCO2 in the regulation of brachial blood flow in humans
Date
2004
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Abstract
This study examined the role of arterial PO2 (PaO2) and PCO2 (PaCO2) in the regulation of brachial blood flow (BBF) in humans.
Nine healthy male subjects participated in five 60-min experimental conditions: isocapnic hypoxia, isocapnic hyperoxia, euoxic hypocapnia, euoxic hypercapnia, and euoxia isocapnia (control). Dynamic end-tidal forcing was used to control end-tidal (i.e., arterial) PO2 and PCO2.
Doppler ultrasound was used to measure BBF. Hypoxia elicited a sustained increase in BBF (25 ± 14%; P<0.05), whereas hyperoxia caused a sustained decrease in BBF (15 ± 8%; PO.05). Hypocapnia elicited a biphasic response, where BBF transiently increased (31 ± 17%; PO.05) after 2 min and abruptly declined (25 ± 14% below baseline) thereafter. During hypercapnia BBF initially increased (14 ± 10%; P<0.05), but returned to baseline values after 20 min.
The present study provides direct evidence that alterations in PaO2 and PaCO2 have dynamic effects on blood flow regulation through the brachial artery.
brachial blood flow, hypoxia, hyperoxia, hypocapnia, hypercapnia, euoxia, isocapnia
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Bibliography: p. 128-152
Some pages are in colour.
Some pages are in colour.
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Citation
Ashmead, J. C. (2004). Role of arterial PO2 and PCO2 in the regulation of brachial blood flow in humans (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/20823