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J Appl Physiol (February 15, 2002). doi:10.1152/japplphysiol.00965.2001
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Articles in PresS, published online ahead of print February 15, 2002
J Appl Physiol, 10.1152/jap.00965.2001
Submitted on September 18, 2001
Accepted on February 8, 2002

Desferrioxamine elevates pulmonary vascular resistance in humans: potential for involvement of HIF-1

George M Balanos1, Keith L Dorrington1, and Peter A Robbins1*

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.

Hypoxia-inducible factor 1 (HIF-1) is stabilized by hypoxia and iron chelation. We hypothesized that HIF-1 might be involved in pulmonary vascular regulation and that infusion of desferrioxamine over 8 h would consequently mimic hypoxia and elevate pulmonary vascular resistance. In study A we characterized the pulmonary vascular response to 4 h isocapnic hypoxia; in study B we measured the pulmonary vascular response to 8 h desferrioxamine infusion. For study A eleven volunteers undertook two protocols: 1) 4 h isocapnic hypoxia (end-tidal PO2 = 50 mmHg), followed by 2 h recovery with isocapnic euoxia (end-tidal PO2 = 100 mmHg); 2) 6 h air-breathing (control). For study B nine volunteers undertook two protocols while breathing air: 1) continuous infusion of desferrioxamine (4 g/70 kg) over 8 h; 2) continuous infusion of saline over 8 h (control). In both studies, pulmonary vascular resistance was assessed at 0.5-1 h intervals using Doppler echocardiography via the maximum pressure gradient during systole across the tricuspid valve. Results show a progressive rise in pressure gradient over the first 3-4 h with both isocapnic hypoxia (p < 0.001) and desferrioxamine infusion (p < 0.005) to increases of approximately 16 and 4 mmHg respectively. These results support a role for HIF-regulated gene activation in human hypoxic pulmonary vasoconstriction.




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