Fig. 2
Arrhythmogenic effect of C18:1AC on contractility of human atrial trabeculae and on single murine ventricular cardiomyocytes. a Force of human right atrial trabeculae after 1 h exposure to 25 µM C18:1AC and 30 min wash-out (mean ± SEM, n = 5/5, number of trabeculae/number of patients). b Representative contraction peaks before and after 1 h of superfusion with C18:1AC at 25 µM. c Number of trabeculae with spontaneous contractions (SC) during 1 min interval without electrical stimulation after C18:1AC exposure and d representative traces with each peak representing one contraction (n = 5, Χ2 tests, *p < 0.05). e Inotropic effect of C18:1AC on human atrial EHT (3.6 Hz, 1.2–1.5 mM Ca2+, n = 8–12/2 per group (number of EHTs/batches), three technically independent experiments) under electrical stimulation in the presence of full SR Ca2+ and after treatment with ryanodine and cyclopiazonic acid to deprive the SR of Ca2+ (Rya + CPA, mean ± SEM, two-way ANOVA plus Bonferroni’s post-test for multiple comparisons, ***p < 0.001 vs. vehicle control). Force normalised to baseline and corresponding vehicle controls (dotted line). f Force normalised to corresponding vehicle control 24 h after washing out C18:1AC. SR = sarcoplasmic reticulum. g Murine ventricular cardiomyocytes were loaded with the calcium-dye Indo-AM to determine cytosolic Ca2+ and were stimulated at 1 Hz. After 120 s, C18:1 or short-chain AC were washed in for 420 s. The increase in diastolic Ca2+ concentration was more pronounced in C18:1AC group compared to the short-chain AC group. h Systolic Ca2+ transients were decreased in the C18:1AC group, compared to the point of origin