Direct inotropic effects of propofol and adenosine on rat atrial muscle: Possible mechanisms

Experiments were designed to evaluate the mechanisms of propofol and adenos ine in rat atrial muscle. Atria were suspended in the isolated organ bath s ystem for isometric tension recording and response to propofol and adenosin e were tested in the absence and presence of glibenclamide, N-G-nitro-argin ine-methyl-ester (L-NAME), tetraethylammonium (TEA) and 8-phenyltheophyllin e (8-PT). The inotropic effect of propofol was elicited by TEA and glibencl amide. In contrast, L-NAME and 8-PT has no effect on the propofol-induced i nhibition of atria. Furthermore, atria exhibited a diminished sensitivity t o the adenosine-induced negative inotropic effect in the presence of the K- ATP channel inhibitor glibenclamide, but not the non-specific K+ channel in hibitor TEA. The adenosine A(1) receptor antagonist 8-PT decreased the resp onsiveness of adenosine-induced inhibition of atrial muscle. We propose tha t propofol-induced inotropy is generally mediated by K+ channels, whereas a denosine-induced inotropy is partially mediated by K+ channels. Both propof ol- and adenosine induced inotropy were not mediated by nitric oxide releas e. Our study provides further evidence that there was no contribution of ad enosine in the propofol-induced inotropy. (C) 2000 Academic Press.