Conjunctival immediate hypersensitivity: re-evaluation of histamine involvement in the vasopermeability response.

The recent development of a technique for quantitative measurement of conjunctival microvascular permeability has permitted detailed pharmacological evaluation of H1- and H2-receptor involvement in histamine-induced increases in conjunctival microvascular permeability and the role of histamine in microvascular permeability changes associated with immediate hypersensitivity responses in the conjunctiva. The conjunctival microvascular permeability response to histamine appears to be entirely mediated by H1-receptors. Pyrilamine (H1-receptor antagonist) virtually abolished the increase in conjunctival extravascular albumin content produced by graded doses of histamine, whereas cimetidine (H2-receptor antagonist) was ineffective. Moreover, selective histamine H2-receptor agonists did not elicit a dose-dependent vasopermeability response in the conjunctiva. Although H1-receptor blockade essentially abolished the microvascular permeability response to histamine, it only partially attenuated the conjunctival microvascular permeability response associated with immediate hypersensitivity and compound 48-80. It appears that conjunctival inflammation caused by mast cell degranulation comprises both a histaminergic and a nonhistaminergic component.