Prostanoids or prostaglandins, the cyclooxygenase metabolites of arachidonate, are synthesised and released in large quantities by such mediator cells as mast cells, neutrophils and macrophages with immunologic activation. Since these inflammatory cells are localised in the airways, prostanoids are attractive candidates as putative inflammatory mediators in the pathogenesis of bronchial asthma. This thesis contrasts the direct airways effect(s), the interaction(s) and the metabolism of inhaled prostaglandins (PG) D₂, F_2α and I₂ in normal and asthmatic subjects. The body plethysmograph was used to measure airways resistance (Raw) and results were expressed as specific airways conductance (sGaw). Forced expiratory volume in one second (FEV₁) and maximum expiratory airflow rate at 30% of vital capacity (Vmax₃₀) were measured using a flow-dependent spirometer, lung volumes in a volume compensated body plethysmograph and lung compliance by oesophageal manometry during a quasistatic full inspiratory and expiratory manoeuvre. Changes in these airway measurements were investigated with inhaled prostaglandin D₂ (PGD₂), prostaglandin F_2α (PGF_2α) and prostaglandin I₂ (PGI₂, prostacyclin). PGD₂ was demonstrated to be a potent bronchoconstrictor four times more potent than PGF_2α in molar equivalents. This observation together with the finding that inhaled PGD₂, unlike PGD_2α, was not significantly converted to conventional prostaglandin F metabolites demonstrates that PGD₂ has its own pharmacological effects not related to its reduction to PGF_2α . A time course method for interacting equiconstrictor concentrations of two bronchoconstrictor agonists, using inhaled adenosine and methacholine as control compounds was devised. Application of this method to the interaction of the two mast cell-derived mediators, histamine and PGD₂ demonstrated an additive airway effect only. The discriminatory nature of sGaw, Vmax₃₀, FEV₁, lung volumes and compliance for detecting bronchoconstriction at different levels of the bronchial tree was also investigated. No difference in the responses of these airway measurements to inhaled PGD₂, histamine and methacholine was observed suggesting that they are not sufficiently specific and selective for different sized airways and that extreme caution should be exercised in ascribing preferential sites of action to bronchoconstrictor agonists on the basis of these measurements alone. Inhaled PGI₂ had no overall effect on airway calibre measured as sGaw in asthmatic and normal subjects, although the individual responses were variable. However, PGI₂ in all asthmatic subjects studied produced concentration-dependent falls in FEV₁ and Vmax₃₀, accompanied by increases in residual volume. Despite its apparent direct airway constrictor activity, inhaled PGI₂ was a potent anti-bronchoconstrictor protecting against bronchoconstriction induced by PGD₂ and methacholine, suggesting functional antagonism. These observations regarding their biological activities are discussed in relation to the possible pathophysiological role of these potent inflammatory mediators in the pathogenesis of bronchial asthma. It is suggested that the pathological findings of a chronic inflammatory cell infiltrate, smooth muscle bronchoconstriction and hypersecretion of mucus, which are characteristic of bronchial asthma, may in part be ascribed to the biological activities of these eicosanoids.