The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels

Figures

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  Scheme 1. Anaesthesia device and airtight chamber system used during 5.1% sevoflurane exposure of cardiomyocyte cells.

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  Figure 1. (A,B) The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on cytosolic calcium levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM, on the 20th cycle) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 3). a p ˂ 0.001 and b p ˂ 0.05 vs. control, c p ˂ 0.001 vs. SEV, d p ˂ 0.001 vs. REM, and e p ˂ 0.05 vs. SEV + REM group.

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  Figure 2. The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on apoptosis levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 vs. control, b p ˂ 0.001 vs. SEV, c p ˂ 0.005 and d p ˂ 0.001 vs. REM, and e p ˂ 0.05 vs. SEV + REM.

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  Figure 3. The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on reactive oxygen and mitochondrial depolarisation levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 and b p ˂ 0.05 vs. control, c p ˂ 0.001 vs. SEV, e p ˂ 0.001 and f p ˂ 0.05 vs. REM, and g p ˂ 0.001 vs. SEV + REM.

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  Figure 4. The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on caspase-3 and caspase-9 levels in the cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 vs. control, b p ˂ 0.001 vs. SEV, c p ˂ 0.001 vs. REM, and d p ˂ 0.001 vs. SEV + REM.