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Endothelin receptor blockade does not improve hypoxemia following acute pulmonary thromboembolism

¹James Hogg iCAPTURE Research Laboratory, University of British Columbia, Vancouver, British Columbia, Canada; Departments of ²Physiology and Biophysics and ³Medicine, University of Washington, and ⁴The Mountain-Whisper-Light Statistical Consulting, Seattle, Washington

Submitted 12 September 2005 ; accepted in final form 10 October 2006

We studied the roles of endothelins in determining ventilation (A) and perfusion () mismatch in a porcine model of acute pulmonary thromboembolism (APTE), using a nonspecific endothelin antagonist, tezosentan. Nine anesthetized piglets (23 kg) received autologous clots (20 g) via a central venous catheter at time = 0 min. The distribution of A and at five different time points (–30, –5, 30, 60, 120 min) was mapped by fluorescent microspheres of 10 different colors. Five piglets (group 1) received tezosentan (courtesy of Actelion) starting at time = 40 min for 2 h, and four piglets (group 2) received only saline and served as control. Our results showed that, in all of the animals at 30 min following APTE but before tezosentan, the mean A/ was increased, as was A/ heterogeneity (log SD A/), which represented a widening of its main peak. Afterwards, tezosentan attenuated the pulmonary hypertension in group 1 but also produced moderate systemic hypotension. However, it did not improve arterial PO₂ or A/ mismatch. We concluded that endothelin antagonism had minimal impact on gas exchange following APTE and confirmed our earlier observation that the main mechanism for hypoxemia in APTE was due to the mechanical redistribution of pulmonary regional blood flow away from the embolized vessels, resulting in the creation of many divergent low and high A/ regions.

cluster analysis; fluorescent microspheres; gas exchange; regional blood flow; regional ventilation