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Articles in PresS, published online ahead of print December 13, 2002
J Appl Physiol, 10.1152/jap.00890.2002
Submitted on September 26, 2002
Accepted on December 6, 2002
1 University Laboratory of Physiology, University of Oxford, Oxford, United Kingdom
* To whom correspondence should be addressed. E-mail: peter.robbins{at}physiol.ox.ac.uk.
Hypercapnia has been shown in animal experiments to induce pulmonary hypertension. This study measured the sensitivity and time course of the human pulmonary vascular response to sustained (4 h) hypercapnia and hypocapnia. Twelve volunteers undertook three protocols: 1) 4 h euoxic (end-tidal PO2=100 mmHg) hypercapnia (end-tidal PCO2 10 mmHg above normal), followed by 2 h recovery with euoxic eucapnia ; 2) 4 h euoxic hypocapnia (end-tidal PCO2 10 mmHg below normal) followed by 2 h recovery; 3) 6 h air-breathing (control). Pulmonary vascular resistance was assessed at 0.5-1 h intervals using Doppler echocardiography via the maximum tricuspid pressure gradient during systole. Results show progressive changes in pressure gradient over 1-2 h after the onset or offset of the stimuli, and sensitivities of 0.6-1 mmHg change in pressure gradient per mmHg change in end-tidal PCO2. The human pulmonary circulatory response to changes on PCO2 has a slower time course and greater sensitivity that is commonly assumed. Vascular tone in the normal pulmonary circulation is substantial.
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