Electroacupuncture mitigates intestinal impairment following cardiac arrest resuscitation in sleep-deprived rats

Background Epidemiological studies have demonstrated that sleep deprivation (SD) is associated with an elevated risk of cardiovascular disease, with cardiac arrest (CA) representing the most severe manifestation. Following cardiopulmonary resuscitation (CPR), in addition to sustaining cardiac and cerebral functions, intestinal dysfunction may contribute to a complex post-resuscitation syndrome. Therefore, the preservation of intestinal function is of critical importance. Electroacupuncture (EA) has demonstrated beneficial effects in the recovery from numerous complex diseases. Our study examines the impact and the mechanism of EA on CA-induced intestinal dysfunction following SD. Methods Sleep-deprived rats (NO. SYDW2023-13) were employed to induce cardiac CA via apnea. The effects of SD and EA on intestinal damage were comprehensively assessed at 96 h after CA. Intestinal flora and common organic acid metabolites were also studied. The effects of EA on intestinal peristalsis, barrier integrity, and inflammatory factor levels were validated through autonomic nerve balance, as demonstrated by vagotomy or sympathetic chemical ablation. Excitatory amino acid transporter 2 (EAAT2) protein expression level in enteric glial cells (EGCs) was quantified through immunofluorescence (IF). The functional effects of EA were examined by modulating EAAT2 activity with an agonist (LDN_212320) or an inhibitor (dihydrocainic acid). Results SD exacerbated intestinal injury following CA and reduced intestinal motility. Conversely, EA mitigated intestinal injury and enhanced intestinal motility. Additionally, EA influenced alterations in intestinal flora and plasma organic acid metabolites. The efficacy of EA was attenuated when sympathetic or parasympathetic nerve activity was inhibited. The inhibition of EAAT2 expression in EGCs attenuated the therapeutic efficacy of EA, whereas the upregulation of EAAT2 expression enhanced its therapeutic effect. Conclusion EA facilitates the expression of EAAT2 in EGCs by modulating autonomic nerve balance, thereby mitigating small intestinal damage induced by CA following SD. Additionally, EA ameliorates dysbiosis of intestinal microflora and disturbances in organic acid metabolism.