Abstract
Experiments were designed to evaluate the mechanisms of propofol and adenosine in rat atrial muscle. Atria were suspended in the isolated organ bath system for isometric tension recording and response to propofol and adenosine were tested in the absence and presence of glibenclamide, NG-nitro-arginine-methyl-ester (l-NAME), tetraethylammonium (TEA) and 8-phenyltheophylline (8-PT). The inotropic effect of propofol was elicited by TEA and glibenclamide. In contrast, l-NAME and 8-PT has no effect on the propofol-induced inhibition of atria. Furthermore, atria exhibited a diminished sensitivity to the adenosine-induced negative inotropic effect in the presence of the KATPchannel inhibitor glibenclamide, but not the non-specific K+channel inhibitor TEA. The adenosine A1receptor antagonist 8-PT decreased the responsiveness of adenosine-induced inhibition of atrial muscle. We propose that propofol-induced inotropy is generally mediated by K+channels, whereas adenosine-induced inotropy is partially mediated by K+channels. Both propofol- and adenosine-induced inotropy were not mediated by nitric oxide release. Our study provides further evidence that there was no contribution of adenosine in the propofol-induced inotropy.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call