Clinically Relevant Concentrations of Propofol Have No Effect on Adenosine Triphosphate–sensitive Potassium Channels in Rat Ventricular Myocytes

Abstract

Propofol had no effect on the sarcolemmal K(ATP) channel activities in patch clamp configurations and the mitochondrial flavoprotein fluorescence induced by diazoxide at clinically relevant concentrations (< 2 microm), whereas it significantly inhibited both K(ATP) channel activities at very high, nonclinical concentrations (> 5.6 microg/ml; 31 microm).

Functional roles of ATP-sensitive potassium channel as related to anesthesia

“…Electrophysiological experiments have shown that isoflurane may activate K ATP channels at a moderately acidic intracellular pH of 6.8 [16] or facilitate the opening of channels via the activation of protein kinase C [17]. In contrast, our previous patch-clamp experiments indicated that high supraclinical concentrations of propofol directly inhibited the cardiac K ATP -channel activity [18,19]. Ketamine also inhibits recombinant cardiac K ATPchannel activity in a concentration-dependent manner [20].…”

Effects of intracellular MgADP and acidification on the inhibition of cardiac sarcolemmal ATP-sensitive potassium channels by propofol

“…Our previous studies demonstrated that propofol directly inhibited native and recombinant cardiac sarcolemmal K ATP channel activities during simulated ischemia [8,9]. These observations suggest that intravenous anesthetics may impair the endogenous organ protective mechanisms mediated by K ATP channels.…”

Anesthetic-induced myocardial protection in cardiac surgery: relevant mechanisms and clinical translation

“…It also provides mitochondrial membrane stabilization via decreased mitochondrial calcium uptake and direct inhibition of mPTP [32]. In contrast to volatile anesthetics and opioids, its mechanism of action suggests that it does not trigger signaling pathways related to pre-or postconditioning, and thus lacks any conditioning effect in terms of myocardial protection against I-R injury [33]. Propofol's ability to preserve myocardial function after I-R injury may be attributable to the compensatory hypercontractile state of the non-ischemic region, whereas isoflurane is able to preserve the contractile function in the ischemic region [34].…”