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. Author manuscript; available in PMC: 2023 May 1.
Published in final edited form as: J Mol Cell Cardiol. 2022 Feb 1;166:11–22. doi: 10.1016/j.yjmcc.2022.01.008

Figure 6. Lack of CD38 reduces the frequency of spontaneous calcium release from the sarcoplasmic reticulum in vitro and diminishes susceptibility to catecholamine induced arrhythmias in vivo.

Figure 6.

(a) Typical space-time plot of spontaneous sarcoplasmic reticulum calcium releases in representative WT and CD38KO cardiomyocytes under stressful conditions ([Ca2+]e = 6 mM). The graphs show frequency of calcium sparks (left) and frequency of both waves and miniwaves (right) in WT and CD38KO cardiomyocytes. Lack of CD38 reduces the frequency of spontaneous calcium release from the sarcoplasmic reticulum. Each point in the graphs represents the average value for all the cells recorded for each mouse (N=3 mice/group, n=8 and 15 cell for WT and CD38KO groups respectively). Data are mean ± SEM analyzed by unpaired two-sided t-test, **P<0.01. (b) Representative 1 second ECG traces obtained from a WT and a CD38KO mice before (basal) and after the injection of caffeine-epinephrine i.p. (120–2 mg/kg respectively) to induce arrhythmia. As shown in the graph, bidirectional ventricular tachycardia (VT) incidence was reduced in CD38KO group (N= 5 mice per group, aged 9-month-old). The bar represents 100 ms. Data are analyzed by Fisher’s exact test. ****P<0.0001.