Effects of inhaled monoethanolamine on bronchoconstriction

We previously reported a 65-year-old man who aspirated an alkaline detergent containing 3.3% w/v (weight of solute per volume of solution) monoethanolamine (MEA) into his lungs, causing asthma-like symptoms. We presently describe the mechanism of MEA-induced bronchoconstriction according to findings in guinea pigs. In anesthetized, artificially ventilated animals, changes in airway opening pressure (P(ao)) were measured as an index of bronchoconstriction. An aerosol of 3.3% MEA solution (0.1 ml kg(-1)) inhaled through a tracheal cannula induced significantly stronger bronchoconstriction than an aerosol of potassium hydroxide (KOH) solution (0.1 ml kg(-1)) at the same pH. MEA-induced bronchoconstriction was significantly suppressed by premedication with intravenously injected atropine sulfate (3 mg kg(-1)), a muscarinic receptor antagonist, or diphenhydramine hydrochloride (10 mg kg(-1)), a histamine-H(1) receptor antagonist. MEA-induced bronchoconstriction was not enhanced by premedication with an intravenous injection of neostigmine (0.1 mg kg(-1)), an acetylcholinesterase inhibitor. When bronchoconstriction was induced by MEA, histamine concentrations in bronchoalveolar lavage fluid (BALF) were not significantly greater than in BALF after KOH-induced bronchoconstriction or in BALF after inhalation of physiologic saline. In vitro, contraction of trachea denuded of epithelium during superfusion with MEA (10 mm) was suppressed by premedication with pyrilamine maleate, a histamine-H(1) receptor antagonist, at 10 and 100 microm. Contraction of trachea denuded of epithelium during superfusion with MEA (10 mm) was suppressed by premedication with atropine sulfate at 10 and 100 microm. These results suggest that asthma-like symptoms may result partly from agonistic MEA effects at histamine-H(1) receptors and muscarinic receptors.