Abstract
In sheep low-dose endotoxin infusion causes transient thromboxane-mediated pulmonary vaso- and bronchoconstriction. These changes are paralleled by a decrease of arterial PO2. To elucidate the mechanisms of hypoxia we analysed ventilation-perfusion (VA/Q) distributions by the multiple inert gas elimination technique before and after endotoxin infusion in six conscious sheep. We found that hypoxia after endotoxin could be explained by both a VA/Q inequality and a simultaneous decrease in the mixed venous oxygen tension. The latter was due to a decrease of cardiac output. True shunt did not contribute to hypoxia as it was unchanged.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have