Does deficiency of the two-pore-domain potassium channel TREK-1 promote hyperoxia-induced lung injury?
TREK-1 deficiency resulted in increased sensitivity of lungs to hyperoxia, but this effect is less prominent if overwhelming injury is induced by the combination of hyperoxia and injurious mechanical ventilation. TREK-1 may constitute a new potential target for the development of novel treatment strategies against hyperoxia-induced lung injury.
I.V. and i.p. lidocaine blunted systemic vascular responses to carbon dioxide pneumoperitoneum in pigs, but without influencing vasopressin release.