RESUMO
CoNiP nanosheet array catalysts were successfully prepared on three-dimensional (3D) graphene foam using hydrothermal synthesis. These catalysts were prepared using 3D Ni-graphene foam (Ni/GF), comprising nickel foam as the 'skeleton' and reduced graphene oxide as the 'skin'. This unique continuous modified 'skeleton/skin' structure ensure that the catalysts had a large surface area, excellent conductivity, and sufficient surface functional groups, which promoted in situ CoNiP growth, while also optimizing the hydrolysis of sodium borohydride. The nanosheet arrays were fully characterized and showed excellent catalytic performance, as supported by density functional theory calculations. The hydrogen generation rate and activation energy are 6681.34 mL min-1 g-1 and 31.2 kJ mol-1, respectively, outperforming most reported cobalt-based catalysts and other precious metal catalysts. Furthermore, the stability of mockstrawberry-like CoNiP catalyst was investigated, with 74.9% of the initial hydrogen generation rate remaining after 15 cycles. The catalytic properties, durability, and stability of the catalyst were better than those of other catalysts reported previously.
RESUMO
UNLABELLED: Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice. Indirect evidence from clinical trials demonstrates that chronic inhibition of the renin-angiotensin-system (RAS) significantly reduces the incidence of AF. Since mechanisms of this protective effect of RAS-blockade are poorly understood, we directly tested proarrhythmic effects of angiotensin II (Ang II) in human atrial myocardium. METHODS: Isolated trabeculae from human atrial appendages (n=80) were electrically stimulated. We assessed isometric force and incidence of arrhythmic extra contractions (AECs) with and without increasing concentrations of Ang II (1-1000 nmol/L) in the absence or presence of receptor-blockade by saralasin (non-specific ATR-antagonist), irbesartan (AT1R-antagonist) or PD123319 (AT2R-antagonist). RESULTS: Twitch force and AECs concentration-dependently increased with Ang II. Effects became significant at concentrations >1 nmol/L Ang II and were maximal at 1000 nmol/L (increase in twitch force to 157+/-14% and AECs from 0 to 80%) saralasin and irbesartan partially prevented the inotropic effect of 100 nmol/L Ang II (by 45+/-12% and 68+/-6%; p<0.05), and completely prevented the occurrence of AECs. CONCLUSION: Ang II exerts direct pro-arrhythmic effects in human atrial myocardium. These effects are mediated by AT1-receptors and can be prevented by AT1R-blockade. This mechanism may contribute to the beneficial effects of RAS-blockade on AF in clinical trials.