Syringic acid inhibits apoptosis pathways via downregulation of p38MAPK and JNK signaling pathways in H9c2 cardiomyocytes following hypoxia/reoxygenation injury.

Syringic acid (SA), a naturally occur-ring O­methy-lated trihydroxybenzoic acid monomer extracted from Dendrobium nobile Lindl., has been demonstrated to attenuate renal ischemia­reperfusion (I/R) injury. However, the role of SA in myocardial I/R injury is unclear. The present study aimed to clarify the cardioprotective effect of SA in myocardial I/R injury in vitro and explore the potential molecular mechanisms. In the present study, it was revealed that pretreatment with SA increased the viability and inhibited oxidant stress in H9c2 cardiomyocytes that had suffered hypoxia/reoxygenation (H/R). SA also markedly downregulated B­cell lymphoma 2 (Bcl­2) expression and inhibited the expression of Bcl­2­like protein 4 (Bax) and cleaved caspase­3 in H9c2 cardiomyocytes induced by H/R. In addition, SA significantly alleviated H/R-induced the phosphorylation of p38 mitogen­activated protein kinase (p38MAPK) and c­Jun N­terminal kinase (JNK) in H9c2 cardiomyocytes. In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. The results support the therapeutic usage of SA in the treatment of myocardial infarction.

Alcohol ablation at the posterior papillary muscle prevents ventricular fibrillation in swine without affecting mitral valve function.

AIMS: Radiofrequency ablation at the posterior papillary muscle (PM) significantly reduced ventricular fibrillation (VF) inducibility in rabbits and dogs, suggesting that PM may be involved in the generation of VF. However, the effect of ablation at the PM on VF inducibility remains unknown in normal intact swine hearts because in this species radiofrequency energy delivered at PM provoked incessant VF. METHODS AND RESULTS: Twelve anesthetized swine underwent median sternotomy. Under the ultrasonographic guidance, chemical ablation was performed via injection of dehydrated alcohol into the base of the posterior PM (group PM, n = 6) or anterior wall (control group, n = 6) in the left ventricle. Ventricular fibrillation inducibility and mitral valve function were measured pre- and post-ablation. Hearts were explanted and the ablated myocardium was stained with haematoxylin and eosin. Ventricular fibrillation inducibility was significantly decreased from 100 ± 0% pre-ablation to 11.9 ± 7.8% post-ablation in group PM (P = 0.001), whereas it was not statistically different in the control group (100 ± 0 vs. 92.9 ± 7.1%, pre-ablation vs. post-ablation). Haemorrhage and cellular necrosis was observed in the centre of ablated myocardium and no significant mitral regurgitation was observed following ablation at the posterior PM. CONCLUSION: Alcohol ablation of the left posterior PM reduced VF inducibility in normal intact swine hearts, with no significant mitral regurgitation. This suggests that the posterior PM may be involved in the generation of VF, and the recurrence of VF may be prevented by chemical ablation at the posterior PM.

Hydrogen sulfide opens the KATP channel on rat atrial and ventricular myocytes.

OBJECTIVE: Hydrogen sulfide (H(2)S), an endogenous gaseous transmitter, was found to protect the heart from various forms of injury, but the underlying mechanism is not known. H(2)S can open the K(ATP) channel on vascular smooth muscle cells, and the objective of this study was to determine whether H(2)S can open the K(ATP) channel on myocardiocytes. METHODS: The whole-cell patch-clamp technique was used to record I(K,ATP) and action potentials of atrial and ventricular myocytes isolated from the hearts of male Wistar rats. Sodium hydrogen sulfide (NaHS) was used as a donor of H(2)S to observe the effect of exogenous H(2)S on I(K,ATP). DL-propargylglycine (PPG), an inhibitor of the synthesis of H(2)S, was used at a concentration of 200 microM to observe the effect of endogenous H(2)S on I(K,ATP). RESULTS: NaHS at concentrations (in microM) of 9.375, 18.75, 37.5, 75 and 150 increased I(K,ATP) by 12.8% (p > 0.05), 28.4% (p < 0.05), 38.8% (p < 0.01), 51.2% (p < 0.01) and 58.6% (p< 0.01) on ventricular myocytes, respectively, and by 6.8% (p > 0.05), 10.4% (p > 0.05), 18.9% (p < 0.01), 24.8% (p < 0.01) and 37.2% (p < 0.01) on atrial myocytes, respectively. The H(2)S-induced decrease in the duration of action potentials (APD(90)) of ventricular myocytes was concentration-dependent, although only NaHS at a concentration of 150 microM decreased the APD(90) significantly (15%, p < 0.05). The H(2)S-induced decrease in APD(90) on atrial myocytes was concentration dependent, but the statistical difference was not significant. Inhibition of I(K,ATP) by PPG was time dependent and the level of inhibition was: ventricular myocytes, 7% (p > 0.05), 10% (p < 0.05), 15.3% (p < 0.01), 24.0% (p < 0.01) and 28.9% (p < 0.01); atrial myocytes, 15.8% (p > 0.05), 21.3% (p > 0.05), 26.5% (p < 0.01), 34.0% (p < 0.01) and 43.2% (p < 0.01) measured at 5, 10, 15, 20 and 25 min, respectively. The increase in the APD(90), by PPG was time dependent for ventricular myocytes [increased by 12.8% (p < 0.05) at 25 min]. The same was true for atrial myocytes, although only the value at 25 min was significant (15%, p < 0.05). CONCLUSIONS: H(2)S decreased the APD(90),and both the endogenous and exogenous H(2)S-induced increase in I(K,ATP) on both atrial and ventricular myocytes was concentration dependent. These results may help to explain, at least in part, how H(2)S protects heart cells from various forms of injury.