Propofol induces dilation and inhibits constriction in guinea pig basilar arteries.

The present study investigated the direct action of propofol on guinea pig basilar arterial rings and the possible underlying mechanisms. Arterial rings, with and without endothelium, were mounted in an organ bath and connected to an isometric tension recording system. The effects of propofol (0.63-20 micrograms/mL) were compared with those of Intralipid (n = 13) after equilibration and precontraction by 5-hydroxytryptamine (5-HT). In another group (n = 8), after pretreatment with either propofol (5 micrograms/mL) or Intralipid, a contraction by 35 mM KCl was obtained and compared. Another group (n = 12) were incubated in Ca(2+)-free Krebs buffer and after depolarization by 45 mM KCl, a dose-response curve to CaCl2 was obtained to compare the effect of propofol (5 micrograms/mL) and Intralipid on the influx of Ca2+. Finally, in Ca(2+)-free Krebs buffer, the effect of Intralipid or propofol on 5-HT-evoked contractions (n = 6) were assessed. Propofol caused significant dilation with or without endothelium present, inhibited KCl-induced contraction, and significantly lowered the dose-response curve for CaCl2. In Ca(2+)-free Krebs buffer, propofol significantly inhibited 5-HT-evoked contraction, which is dependent on intracellular Ca(2+)-release. In conclusion, propofol inhibited vaso-constriction and induced vasodilation by mechanisms consistent with reduced extracellular calcium influx and suppressed intracellular calcium release.