Propofol enhances a d-tubocurarine-induced twitch depression in septic ratdiaphragm

We estimated the effect of d-tubocurarine (dTc) on neuromuscular transmissi on and the action of propofol on dTc-induced twitch depression by using sha m control and septic rat nerve-hemidiaphragm preparations in vitro. Isometr ic twitch tension elicited by indirect (phrenic nerve) or direct (muscle) s timulation at 0.1 Hz was evaluated. Sepsis induced by panperitonitis attenu ated the twitch tension elicited by indirect and direct stimulation (P < 0. 01 in each group) in the absence of significant morphological inflammatory damage to the diaphragm. dTc (1 mu M) decreased the twitch tension elicited by indirect stimulation (P < 0.01) less intensely in the septic group than in the sham group (P < 0.01). Propofol accentuated dTc-induced depressed t witch more intensely in the septic group (P < 0.01 or 0.05). These results demonstrate that sepsis attenuates both muscle contractile force and the ef fect of a neuromuscular blocker and that propofol more intensely enhances d Tc-induced twitch depression during sepsis. Implications: Propofol and nond epolarizing muscle relaxants are widely used for various clinical cases, in cluding sepsis. Interactions between nondepolarizing muscle relaxants and p ropofol during sepsis are interesting from a clinical point of view. We dem onstrated that propofol significantly enhances d-tubocurarine-induced twitc h depression in vitro in the septic rat model compared with that in the non septic rat model.