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. Author manuscript; available in PMC: 2010 Sep 8.
Published in final edited form as: Anesthesiology. 2010 Mar;112(3):623–630. doi: 10.1097/ALN.0b013e3181cf894a

Fig. 1.

Fig. 1

KATP channels are activated by xenon. (A) Whole cell recording (holding potential [VH] −20 mV) from an HEK293 cell-expressing Kir6.2/SUR1 channels demonstrating reversible current activation by 80% xenon and its preclusion by tolbutamide (Tb). Drugs were bath applied as indicated by horizontal bars. Dashed line is zero-current level. (B, C) Current–voltage relationships demonstrating KATP current activation by xenon and block by tolbutamide. (D) Mean current amplitude at −20 mV for untransfected and Kir6.2/SUR1-transfected cells in the absence or presence of 80% xenon (Xe). (E) Effects of the SUR1-specific K-channel opener diazoxide (Dz) on Kir6.2/SUR1 whole cell currents. Plotted is the mean holding current at −20 mV every 15 s. (F) Mean effects of the K-channel openers xenon and diazoxide and the blocker tolbutamide on Kir6.2/SUR1 currents. Expressed is the holding current at −20 mV in the presence of the drug as a fraction of the current in the absence of the drug. Xe + Tb: current in the presence of xenon and tolbutamide. Numbers (N) are given above the bars. **P < 0.01 compared with control. ##P < 0.01 compared with lower drug concentration.