Impairment of gas exchange due to alveolar oedema during xylazine sedation in sheep; absence of a free radical mediated inflammatory mechanism.

We studied the mechanism of impairment of gas exchange following sedation with the alpha2 adrenoreceptor agonist, xylazine, in Suffolk cross-bred sheep spontaneously breathing room air. Xylazine caused a significant fall in PaO2 from a mean (pre-xylazine) of 97.9 mm Hg (6.7 mm Hg SEM) to a mean of 38.1 mm Hg (3.2 mm Hg SEM) one minute after injection with a transient increase in PaCO2 from a mean (pre-xylazine) of 32.6 mm Hg (1.9 mm Hg SEM) to a mean of 40.2 mm Hg (3.0 mm Hg SEM). There was no significant fall in mean arterial pressure or in white cell count. There was no significant change in a number of indices of free radical release which included ascorbyl radical, plasma antioxidant potential and alpha-tert-butyl phenyl nitrone (PBN) spin adduct measured simultaneously in both arterial and venous blood. In all sheep given xylazine there was no histological evidence of platelet emboli but lung histopathology showed evidence of pulmonary oedema and intense microvascular congestion with red cells extravasated into alveoli. No such histological changes were seen in the lungs of normal sheep. The impaired gas exchange during sedation with xylazine in sheep is caused, not by an oxidant mediated inflammatory mechanism or by platelet emboli, but by intense alveolar oedema which is probably due to pulmonary venospasm.