FIGURE 3.

Cardiac function and heart rate in cRyr2Δ50 mice. A and B, isolated cardiomyocytes were assessed for average diastolic length (A) and fractional shortening (B) upon stimulation (n = 3; *, p ≤ 0.05.). C and D, isolated cardiomyocyte contraction rate reported as time to 50% peak contraction (C) and time to 50% peak relaxation (D). White circles = control; black circles = cRyr2Δ50. E–G, cardiac output (E), rate pressure product (F), and cardiac work (G) measured during working heart perfusions (control n = 10, cRyr2Δ50 n = 13; *, p ≤ 0.05.). White bars = control; black bars = cRyr2Δ50; throughout. Echocardiograms of control and cRyr2Δ50 mice 3 weeks following tamoxifen treatment are shown. BPM, beats per minute. H and I, average cardiac output (H) and fractional shortening (I) of control and cRyr2Δ50 mice 3 and 20 weeks following tamoxifen treatment (n = 5). J, average heart rate from implantable ECG radio telemetry. Blue points denote days prior to tamoxifen injections (red points), but following surgical recovery and the removal of analgesics. Heart rate is normalized to the average heart rate measured during baseline (gray dashed line). The red dashed line denotes average heart rate of the total cRyr2KO mice reported in our previous publication (4) K, average heart rate before and after tamoxifen treatment (mean ± S.E.; n = 5; *, p ≤ 0.05). All data were plotted as mean ± S.E. Control = Ryr2^{flox/wildtype} + tamoxifen; cRyr2Δ50: Ryr2^{flox/wildtype} × Mhy6-MerCreMer⁺ + tamoxifen.