Skip to main content
. Author manuscript; available in PMC: 2008 Jul 1.
Published in final edited form as: J Mol Cell Cardiol. 2007 Apr 10;43(1):27–38. doi: 10.1016/j.yjmcc.2007.04.002

Fig. 1. Early MAP shorting induced by hypoxia is abolished in AAA-TG mice.

Fig. 1

A. A representative time course of MAP duration during hypoxia. In WT hearts, removal of O2 from the perfusate (application of N2; Inline graphic) leads to an early, presumably IK1-dependent, abbreviation of MAP (2; Inline graphic) followed by a further rapid MAP shortening (3; Inline graphic), presumably due to the activation of KATP channels. The time for early MAP shortening was defined as the time when MAPD75 falls by ∼10% of the Ctrl value measured just before application of N2 (1; Inline graphic). The early phase of MAP shortening is absent in AAA-TG hearts, and only the rapid phase is observed, which starts at the same time as the KATP-dependent phase of MAP shortening in WT hearts (3; Inline graphic). B. Representative MAPs from WT (gray) and AAA-TG (black) hearts recorded at the times as indicated in A. MAP amplitudes were normalized to each other to highlight the differences in shape. C, D. MAPD75 measured at the times as indicated in A. At the time when the early MAP shortening has just begun in AAA-TG hearts (3), in WT hearts MAPD75 has been already reduced by 28%. Statistical significance is indicated compared to MAPD75 before application of N2 (1). D. The time delay (Dt) between the application of N2 and the time when MAPD75 is decreased by 10% in WT and AAA-TG hearts. n=4 for both WT AAA-TG hearts.