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

introductionSevoflurane may exert cytotoxic effects in some cell types, but its impact on human cardiomyocytes and the potential protective role of remifentanil remain unclear. This study aimed to investigate whether remifentanil mitigates sevoflurane-induced apoptotic damage in human cardiomyocytes, with an exploratory focus on TRPA1 calcium channels. MATERIALS AND

methodsHuman cardiomyocyte cells were exposed to sevoflurane (5.1% for 6 h) and/or remifentanil (2.5 µM for 30 min), with or without the TRPA1 antagonist AP18. Apoptosis, intracellular reactive oxygen species (ROS), mitochondrial depolarisation, caspase-3 and -9 activities, and cytosolic calcium levels were measured.

resultsSevoflurane exposure was associated with increased apoptosis, ROS production, mitochondrial depolarisation, caspase-3 and -9 activities, and intracellular calcium levels compared with the control group. Remifentanil pretreatment appeared to reduce these sevoflurane-related changes. In several parameters, the addition of AP18 partially reversed the effects of remifentanil, suggesting that TRPA1 channels may contribute to these effects. However, findings were not entirely consistent across all measured variables.

conclusionsRemifentanil effectively mitigates sevoflurane-induced apoptotic damage in human cardiomyocytes, likely by modulating oxidative stress and preserving mitochondrial function. The partial reversal by AP18 suggests that TRPA1 channels may contribute to these protective effects, though additional mechanisms are likely involved. Further mechanistic and translational studies are warranted to elucidate the precise signalling pathways and clinical relevance of these observations.