Autonomic-cyclooxygenase-2 Mechanisms of Electroacupuncture on Thermal Injury-induced Gastric Dysmotility in Rats.

BACKGROUND AND OBJECTIVES

Gastrointestinal dysmotility commonly follows thermal injuries, such as burns. This study aimed to investigate the effects and mechanisms of electroacupuncture (EA) on burn-induced gastric dysmotility in rats.

METHODS

Sprague-Dawley rats were divided into sham and thermal injury groups subjected to a 60% scald burn. Antagonists, including β-blockade (propranolol), α-blockade (phentolamine), or a selective cyclooxygenase (COX)-2 inhibitor (nimsulide), were administered to verify the pathways involved. Six hours after the burn, the animals were evaluated for gastric emptying and heart rate variability. Blood and gastric tissues were collected for assays of cytokines, hormones, and COX-2 levels. EA was performed at bilateral ST36 (Zusanli) acupoints for 45 m.

RESULTS

Burn injury delayed gastric emptying by 61% ( < 0.01), which was normalized by nimsulide or propranolol but not by phentolamine. EA improved gastric emptying by 87% ( = 0.03) in burned rats. Heart rate variability and plasma hormone (noradrenaline and pancreatic polypeptide) analyses indicated sympathetic hyperactivity in burned rats; EA improved burn-induced sympathovagal imbalance by enhancing vagal activity. Protein and mRNA expressions of COX-2 in the gastric fundus and antrum increased with burn but were normalized by propranolol. EA reduced the burn-induced increase in COX-2 expression in the gastric fundus but not in the antrum. EA also decreased burn-induced elevations in plasma interleukin (IL)-6 and IL-10. Negative correlations were found between gastric emptying and plasma IL-6 levels, as well as between gastric emptying and COX-2 mRNA levels.

CONCLUSIONS

These findings suggest that burn-induced gastric dysmotility is mediated via autonomic-COX-2 pathways. EA at acupoint ST36 improves burn-induced delays in gastric emptying by down-regulating COX-2 and pro-inflammatory cytokines through the autonomic nervous pathway.