We investigated the role of histamine H1- and H2-receptors in the control airway function in six conscious sheep. In five of these, inhalation of histamine (combined H1- and H2-receptor stimulation) caused an increase in pulmonary resistance (R(L)) and functional residual capacity and had a variable effect on distribution of ventilation as measured by N2-clearance delay. Pretreatment with the H1-antagonist, chlorpheniramine, prevented these functional effects of histamine challenge, whereas pretreatment with the H2-antagonist, metiamide, potentiated the effects of histamine on R(L) and caused a uniform increase in N2-clearance delay. Pretreatment with both chlorpheniramine and metiamide prevented the effects of histamine on all parameters indicating effective blockade of H1- and H2-receptors at the dosages used. In one sheep, an increase in R(L) and N2-clearance delay in response to histamine was only observed after metiamide pretreatment. With or without pretreatment, histamine failed to alter the static pressure-volume curve of the lung. We conclude that in conscious sheep a) inhalation of histamine produces bronchoconstriction and pulmonary hyper-inflation without changing lung elastic recoil, b) the observed effects of histamine are mediated by H1-receptors, and H2-receptors have a modulating role, and c) variable effects of histamine on R(L) and distribution of ventilation may be related to differences in the distribution of H1- and H2-receptors in central and peripheral airways.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Applied Physiology Respiratory Environmental and Exercise Physiology|
|State||Published - Jan 1 1980|
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