Why the study?
Cardiac autonomic rebalancing is an important therapeutic strategy for myocardial infarction-produced ventricular arrhythmias, but the role of the parasympathetic-activating short-chain fatty acid propionate was unclear.
Does oral propionate supplementation reduce susceptibility to ventricular arrhythmias in a rat model of myocardial infarction?
Does oral propionate supplementation reduce susceptibility to ventricular arrhythmias in a rat model of myocardial infarction?
Oral propionate supplementation protects against MI-induced ventricular arrhythmias and electrical instability in rats via parasympathetic activation.
Propionate may attenuate post-MI ventricular arrhythmias in rats; leaves open clinical translation of SCFA supplementation.
The short-chain fatty acid (SCFA) propionate (C3), a microorganism metabolite produced by gut microbial fermentation, has parasympathetic-activation effects. The cardiac autonomic rebalancing strategy is considered as an important therapeutic approach to myocardial infarction (MI)-produced ventricular arrhythmias (VAs). Thus, our research was designed to clarify the potential functions of the SCFA propionate in VAs and cardiac electrophysiology in MI rats. A hundred adult Sprague-Dawley rats were allocated to four groups: the sham group (200 mM sodium chloride), the sham + C3 group (200 mM propionate), the MI group (200 mM sodium chloride) and the MI + C3 group (200 mM propionate). In comparison with the sham group, propionate significantly increased the parasympathetic components heart rate variability (HRV) and acetylcholine levels, prolonged cardiac repolarization, induced STAT3 phosphorylation and up-regulated the c-fos expression in nodose ganglia and solitary nucleus. Propionate intake reduced the susceptibility to VAs. MI induced by coronary ligation caused a significant increase in the sympathetic components HRV, abnormal repolarization, global repolarization dispersion, norepinephrine and inflammatory cytokines, reduction and redistribution of Connexin 43 in the infarcted border zone, and activation of NFκB, which were attenuated in the MI + C3 group. Oral propionate supplementation, as a nutritional intervention, protected the heart against MI-induced VAs and cardiac electrophysiology instability partly by parasympathetic activation based on the gut-brain axis.
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Zhou et al. (2021) studied this question.
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