Control of breathing in XXXX . The effect of @entity112 inhalation.

@entity1 @entity112 @entity1030
In 7 normocapnic and 6 hypercapnic @entity1 with @entity1030 ( @entity1030 ), we confirmed the recently reported observation that hypercapnic and/or hypoxemic @entity1 with @entity1030 breathe with a shorter inspiratory time (TI) and a smaller tidal volume (VT) than normocapnic and/or normoxemic @entity1 with @entity1030 . Both hypercapnic and normocapnic groups were exposed to doubling concentrations of aerosolized @entity112 , and FEV1 was measured 30 and 90 s after each 2-min exposure. A provocative concentration (PC20) of @entity112 was defined as that which produced a 20% decrease in FEV1. At PC20, minute ventilation and VT decreased in both groups. The decrease in VT was significantly greater in the normocapnic @entity1 . Inspiratory flow (VT/TI) did not change in either group. Although breathing frequency (f) and inspiratory time (TI) did not change in the hypercapnic group, f increased and TI decreased significantly in the normocapnic @entity1 . The same results were obtained when @entity1 were separated into hypoxemic and "normoxemic" groups. At PC20, therefore, the pattern of breathing of the hypercapnic and/or hypoxemic @entity1 showed only small variations, whereas in the normocapnic and/or "normoxemic" @entity1 , the breathing pattern showed greater changes, becoming similar to that of the hypercapnic and/or hypoxemic @entity1 during control breathing. We speculated, therefore, that activation of @entity112 -sensitive receptors in the airways could be involved in the pathophysiology of the rapid shallow breathing present at rest in hypercapnic and/or hypoxemic @entity1 with @entity1030 .
