In normal subjects inhalation of PGF2α produced two qualitatively different airways responses. In five subjects there was a significant fall in SGaw without change in maximum expiratory flow rates, FEV1 or CV. In contrast, the remaining three subjects showed a significant fall in flow rates and FEV1 together with a significant increase in CV while their SGaw was unaffected. PGF2α inhalation in six asthmatic patients produced a significant fall in maximum expiratory flow rates, FEV1 and SGaw. These patients showed a dual response with individual variability in magnitudes of changes. It is suggested that differing responses may reflect the balance between the sympathetic and parasympathetic nervous controls of the airways, and that the diminished β-receptor activity in asthmatic patients may account for heightened bronchoconstrictor response to inhaled PGF2α both centrally and peripherally in the bronchial tree.
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