Role of α2 receptor in dexmedetomidine-induced improvement in intestinal barrier dysfunction in rats with traumatic brain injury

Abstract

Objective To evaluate the role of α2 receptor in dexmedetomidine-induced improvement in intestinal barrier dysfunction in rats with traumatic brain injury (TBI). Methods Forty clean-grade healthy Wistar rats, aged 12 weeks, weighing 200-250 g, were divided into 4 groups (n=10 each) using a random number table method: control group (group C), TBI group (group T), dexmedetomidine group (group D) and dexmedetomidine plus atipamezole group (group D+ A). Traumatic brain injury model was established by a 20 g weight free fall impact method in chloral hydrate-anesthetized rats.At 30 min before establishing the model, rats were fed 4.0 kD fluorescein-isothiocyanate-conjugated dextran (FITC-Dex) 60 mg/100 g. Dexmedetomidine 50 μg/kg was injected intraperitoneally at 30 min before establishing the model in D and D+ A groups.Atipamezole 500 μg/kg was injected intraperitoneally at 10 min before injecting dexmedetomidine in group D+ A.Blood samples from common carotid artery were obtained at 6 h after establishing the model for determination of concentrations of epinephrine (E) and norepinephrine (NE) in plasma (by enzyme-linked immunosorbent assay), concentrations of FITC-Dex in serum (using fluorescence spectrophotometry) and activity of diamine oxidase (DAO) in serum (by colorimetry). The small intestine was removed for determination of DAO activity (by colorimetry) and for detection of the expression of tight junctional protein zonula occludens-1 (ZO-1) in the intestinal mucosa of epithelial cells. Results Compared with group C, the concentrations of E and NE in plasma, and FITC-Dex concentration and DAO activity in serum were significantly increased, the DAO activity in intestinal tissues was decreased, and the expression of ZO-1 was down-regulated in T, D and D+ A groups (P<0.05). Compared with group T, the concentrations of E and NE in plasma, and FITC-Dex concentration and DAO activity in serum were significantly decreased, the DAO activity was increased, and the expression of ZO-1 was up-regulated in group D (P<0.05). Compared with group D, the concentrations of E and NE in plasma, and FITC-Dex concentration and DAO activity in serum were significantly increased, the DAO activity was decreased, and the expression of ZO-1 was down-regulated in group D+ A (P<0.05). Conclusion α2 receptor is involved in dexmedetomidine-induced improvement in intestinal barrier dysfunction in rats with TBI. Key words: Receptors, adrenergic, alpha; Dexmedetomidine; Craniocerebral trauma; Intestinal mucosa