The potential use of intralipid to minimize propofol's cardiovascular effects.

摘要

To the EditorMany reports exist which advocate the use of intralipid to reverse local anesthetic cardiovascular toxicity. The precise mechanism of action, while unknown at the present time, may include a combination of reduced tissue binding of local anesthetic by a plasma-lipid phase and a beneficial metabolic effect involving cardiac mitochondria.We hypothesized that intralipid can also function as a cardiovascular reversal agent for propofol.Despite suggestions that physostigmine2 or aminophyl-line 3 can reverse the sedative-hypnotic effects of propofol, no medication currently exists which can directly reverse the cardiovascular effects of propofol. It remains a matter of supportive management while allowing the effects of propofol to dissipate. From a recent study involving aging of resistance systemic arteries ex vivo, we found that vascular relaxation was induced by propofol concentrations between 1 and 100 (mu) (unpublished results). In a similar experiment, we also found that propofol-induced relaxation [100 (mu)M (0.02 mg ml-1 final concentration); Novopharm, ON, Canada] was antagonized by the administration of intralipid 20% at a final concentration of 2-4% soybean oil (Baxter, ON, Canada). Our method of isolating arteries has been described previously. Briefly, rat mesenteric arteries 100-200 (mu)m in diameter were excised and subjected to isometric tension studies utilizing a wire myograph system. These arteries were pre-constricted with phenylephrine (PE) and were relaxed by propofol. After the addition ofpropofol (0.02 mg ml~(-1) final concentration), intralipid 20% (500-1,000 (mu)l in 5 ml tissue bath) consistently reversed the relaxation caused by propofol in four out of four samples. In contrast, the addition of an equivalent volume of saline (control) did not reverse the propofol-induced relaxation (Fig. 1). Based on these preliminary findings, we extrapolated that approximately 50-100 ml of intralipid 20% may be required to reverse the effects of 1 ml of commercially available propofol (10 mg ml~(-1)). Additionally, intralipid itself did not induce constriction in the absence of PE and was not toxic to the arteries, since they exhibited PE constriction following intralipid washout.