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. Author manuscript; available in PMC: 2012 Dec 2.
Published in final edited form as: Biochem Biophys Res Commun. 2011 Nov 3;415(4):637–641. doi: 10.1016/j.bbrc.2011.10.125

Figure 1. Reduction in functional KATP channels translates into slowed APD shortening in response to hypoxia.

Figure 1

A. Summary plots of beat-to-beat MAP duration shortening (ΔAPD90) following initiation of hypoxia in isolated, perfused hearts from WT (n=4), Tg[CX1-eGFPKir6.1AAA] (n=3), and Tg[αMHC-αMHC-Kir6.1AAA] vs. WT and Tg[CX1-eGFP-Kir6.1AAA] controls). Also graphed is the response in glyburide (10μM) treated hearts from WT mice (n=5, *p<.05 vs. WT hearts not treated with glyburide). Symbols with error bars mark the mean±S.E for each 40th APD. B. Representative examples of MAPs recorded from WT, Tg[CX1-eGFP-Kir6.1AAA], Tg[αMHC-Kir6.1AAA] and glyburide treated WT hearts paced at 130 ms cycle length. MAPs at baseline and after 30 and 60 seconds of hypoxia are superimposed for comparison. Horizontal dotted lines indicate 90% repolarization. C. Summary statistics showing the half time (t½) of the ΔAPD90 response (*p<.05 for Tg[αMHCKir6.1AAA] vs. combined WT and Tg[CX1-eGFP-Kir6.1AAA] controls). D. Summary statistics showing the area under the curve (AUC) of the ΔAPD90 time course (*p<.05 for Tg[αMHCKir6.1AAA] and glyburide-treated WT vs. combined WT and Tg[CX1-eGFP-Kir6.1AAA] controls).