RESUMEN
In clinical practice, operative stress varies from surgeries, which may lead to many injuries such as ischemia-reperfusion injury (IRI), hyperactivation of sympathetic nervous system (SNS), post-traumatic immunosuppression (PTI), hypercoagulation and inflammation. Acupuncture is effective and advantageous in regulating the stress response to surgery. The great progress has been made in recent years of acupuncture research in postoperative visceral IRI, SNS hyperactivation, PTI, hypercoagulation and inflammation. By collecting the relevant evidences of acupuncture in this field, the application value of acupuncture involved in modulating surgical stress response and the progress of mechanism research are explored and summarized.
Asunto(s)
Terapia por Acupuntura , Daño por Reperfusión , Humanos , Daño por Reperfusión/terapia , InflamaciónRESUMEN
Electroacupuncture (EA) can effectively reduce surgical stress reactions and promote postoperative recovery, but the mechanisms remain unclear. The present study aims to examine the effects of EA on the hyperactivity of the hypothalamicâpituitaryâadrenal (HPA) axis and investigate its potential mechanisms. Male C57BL/6 mice were subjected to partial hepatectomy (HT). The results showed that HT increased the concentrations of corticotrophin-releasing hormone (CRH), corticosterone (CORT), and adrenocorticotropic hormone (ACTH) in the peripheral blood and upregulated the expression of CRH and glucocorticoid receptors (GR) proteins in the hypothalamus. EA treatment significantly inhibited the hyperactivity of the HPA axis by decreasing the concentration of CRH, CORT, and ACTH in peripheral blood and downregulating the expression of CRH and GR in the hypothalamus. Moreover, EA treatment reversed the HT-induced downregulation of oxytocin (OXT) and oxytocin receptor (OXTR) in the hypothalamus. Furthermore, intracerebroventricular injection of the OXTR antagonist atosiban blocked the effects of EA. Thus, our findings implied that EA mitigated surgical stress-induced HPA axis dysfunction by activating the OXT/OXTR signaling pathway.