XXXX -induced @entity358 in lung vascular injury.

@entity308 @entity871 @entity1219 @entity26 @entity1808 @entity9266 @entity651 @entity1617 @entity519 @entity358 @entity35 @entity37999 @entity934
Recent work with isolated blood vessels has emphasized the importance of intact endothelium when the relaxation of vascular smooth muscle is induced by @entity934 ( @entity1617 ). However, the physiologic significance of this endothelial-dependent @entity1617 response in a complete organ circulation is unclear. We questioned whether diminished @entity1617 vasodilation would result from damage of lung vascular endothelium and whether this response could be used as an indication of endothelial injury. We therefore induced @entity651 in one @entity35 model by repeated injections of @entity37999 (ANTU) and in a second @entity35 model by exposing @entity35 for 52 h to 100% @entity26 at a barometric pressure of 760 torr ( @entity871 ). @entity35 injected with @entity9266 , the solvent for ANTU, or exposed to ambient Denver air served as the respective control animals. The isolated lungs of these @entity35 were perfused with a recirculating cell- and plasma-free, physiological salt solution to study the effect of @entity1617 or @entity1219 infusion on pulmonary perfusion pressure and vascular responsiveness. ANTU-treated @entity35 demonstrated an intact vasodilatory response after @entity1617 infusion when compared with the solvent control animals. The immediate @entity358 after @entity1617 infusion was slightly enhanced in the hyperoxic @entity35 lung when compared with the @entity35 exposed to ambient air, but there was no difference between these groups in the prolonged @entity308 of vascular responsiveness to @entity519 or @entity1808 . Thus, in both models of lung endothelial cell injury, the pulmonary vascular responses to @entity1617 were intact.(ABSTRACT TRUNCATED AT 250 WORDS)
