The short-chain fatty acid propionate improved ventricular electrical remodeling in a rat model with myocardial infarction. Issue 24 (23rd November 2021) - Zhou, Mingmin
Abstract : Oral propionate activated vagal afferent nerve in the gut and facilitated solitary nucleus in the brain via nodose ganglia to activate vagal efferent nerve innervating the heart, so as to reduce ventricular arrhythmia after myocardial infarction. Abstract : 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.