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Adrenergic receptor interaction with isoflurane was studied in an in vitro rat parotid gland model in which beta-adrenoceptor agonists evoke amylase release and alpha-adrenoceptor agonists induce potassium secretion from parotid cells. The amylase secretory studies were performed using a batch-incubation technique, and potassium efflux was evaluated using 86Rb+ as a probe for K+. Isoflurane was dissolved in a fat emulsion, which of its own had no secretory effect. Isoflurane induced a dose-dependent amylase release that was unaffected by beta-adrenergic blockade with propranolol and metoprolol. Isoflurane also induced a significant efflux of 86Rb+ that could not be inhibited by the alpha-adrenoceptor antagonist, phentolamine. Dinitrophenol, an uncoupler of oxidative phosphorylation, had no effect on the isoflurane-induced enzyme release, indicating that amylase secretion occurred by passive leakage. It is suggested that isoflurane has no direct action on alpha- or beta-adrenoceptors. Isoflurane, however, induces potent cellular events that might be due to an unspecific effect on the cell membrane, thereby causing changes in membrane permeability.

Isoflurane—A Study of Its Adrenoceptor Interaction in the Isolated Rat Parotid Gland