Vasodilator and constrictor responses to @entity519 in isolated XXXX lungs.

@entity1707 @entity72908 @entity26 @entity519 @entity544
We examined transient and steady-state responses of the pulmonary circulation to @entity519 in isolated @entity1707 lungs perfused with autologous blood. Responses were quantified by the pulmonary artery pressure at a flow of 1 l/min ( @entity72908 ) read directly from pressure-flow recordings. Alveolar @entity544 tension was constant at 38 Torr and alveolar @entity26 pressure (PAO2) was varied between 670 and 0 Torr. When PAO2 was lowered progressively every 10 min, the relation between PAO2 and @entity72908 was sigmoidal, with maximum constriction occurring at a PAO2 of 0 Torr; however, if @entity72908 was allowed to reach a steady state at each level of PAO2, the relation was reproducibly and reversibly biphasic. @entity72908 increased as PAO2 decreased from 670 to 60 Torr, was maximum and stable at PAO2 between 60 and 30 Torr, and decreased as PAO2 was lowered from 30 to 0 Torr. As a result, steady-state @entity72908 at PAO2 greater than or equal to 200 Torr was similar to that at PAO2 = 0 Torr. When PAO2 was changed from 200 Torr to a constant lower level, @entity72908 required 20-30 min to achieve a steady state at PAO2 greater than or equal to 25 Torr and 40-50 min at PAO2 of 10 and 0 Torr. With the latter, the responses consisted of vasoconstriction followed by marked vasodilation. Thus pulmonary vasomotor tone was a complex function of both PAO2 and time. Attempts to explain the pulmonary vascular response to @entity519 must take these complexities into account.
