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. 2020 Jan 24;318(3):H566–H580. doi: 10.1152/ajpheart.00739.2018

Fig. 2.

Fig. 2.

Tandem pore domain acid-sensitive K+ channel 1 (TASK-1) global knockout (KO) mice are resistant to pressure overload cardiomyopathy. Serial echocardiographic measurements of average %fractional shortening [(end-diastolic dimension – end-systolic dimension)/end-diastolic dimension × 100; A], average end-systolic dimension (mm; B), average end-diastolic dimension (mm; C), and average calculated LV mass (mg; D) in TASK-1 KO and wild-type mice at baseline (Base) and up to 12 wk after transverse aortic constriction (TAC). Error bars reflect means ± SE; n = no. of mice. Statistical comparisons between wild-type TAC and TASK-1 KO TAC data were made using two-way repeated measures ANOVA. The P values for the interaction between genotype and weeks post-TAC are shown. Comparisons between genotypes at each time point were made using Bonferroni’s test for multiple comparisons, *P < 0.05 vs. wild-type TAC at each time point. NS, not significant. Average left ventricular (LV) weight-to-tibia length ratio (E) and average left atrial (LA) weight-to-tibia length ratio (F) after Sham or TAC in wild-type and TASK-1 KO mice. Invasively assessed average cardiac output (μL/min; G) and time constant of left ventricular isovolumic relaxation (τ) calculated by the Glantz method (ms; H) after Sham or TAC in wild-type and TASK-1 KO mice. Statistical comparisons between groups in both chamber weights and invasive hemodynamics were made using one-way ANOVA with Bonferroni’s test for multiple comparisons, *P < 0.05 vs. wild-type Sham, †P < 0.05 vs. wild-type TAC.