Objective To evaluate the relationship betweenα2 adrenergic receptors and expression of Nav1. 8 in dorsal root ganglion (DRG) neurons, and to illuminate the mechanism of dexmedetomidine-induced reduction of acute visceral pain in rats. Methods Thirty-two clean-grade healthy adult male Spra-gue-Dawley rats, aged 6-8 weeks, weighing 180-220 g, were divided into 4 groups ( n=8 each) using a random number table method: control group ( group C ) , acute visceral pain group ( group VP ) , dexmedetomidine group (group D), and dexmedetomidine plus atipamezole group (group DA). In VP, D and DA groups, 10-3 mmol∕L capsaicin 1. 3 ml was injected into the rectum at a dose of 10-3 mmol∕L to establish the acute visceral pain model, while the equal volume of normal saline was given instead in group C. Atipamezole 1 mg∕kg was subcutaneously injected through the back of the neck at 20 min before establishing the model in group DA. Dexmedetomidine 10μg∕kg was injected through the tail vein at 15 min before establishing the model in D and DA groups, while the equal volume of normal saline was given instead at the correspording time points in C and VP groups. The visceral pain behavior score was recorded at 1 h after establishing the model. The animals were then sacrificed, and DRGs of the lumbar segment (L3-6) were removed for determination of the number of Nav1. 8 positive DRG neurons (by immunohisto-chemistry) and expression of Nav1. 8 mRNA (by quantitative real-time polymerase chain reaction). Results Compared with group C, the visceral behavior scores and the number of Nav 1. 8 positive DRG neurons were significantly increased, and the expression of Nav 1. 8 mRNA was up-regulated in VP, D and DA groups (P<0. 05). Compared with group VP, the visceral behavior score and the number of Nav1. 8 positive DRG neurons were significantly decreased, and the expression of Nav 1. 8 mRNA was down-regulated in D and DA groups (P<0. 05). Compared with group D, the visceral behavior scores and the number of Nav1. 8 positive DRG neurons were significantly increased, and the expression of Nav1. 8 mRNA was up-regulated in group DA ( P<0. 05) . Conclusion The mechanism by which dexmedetomidine reduces acute visceral pain is related to activatingα2 adrenergic receptors and to down-regulating the expression of Nav1. 8 in DRG neu-rons of rats.

Objective To investigate the effect of dexmedetomidine pretreatment on inflammatory visceral pain in rats. Methods Forty healthy male Wistar rats, weighing 200-300 g, aged 6-8 weeks, were divided into 5 groups ( n=8 each) using a random number table method: control group ( group C) , visceral pain group ( group VP ) , dexmedetomidine 1 μg∕kg group ( group Dex1 ) , dexmedetomidine 5μg∕kg group ( group Dex2) and dexmedetomidine 10μg∕kg group ( group Dex3) . The model of inflammato-ry visceral pain was established by intraperitoneally injecting 0. 9％ acetic acid 10 ml∕kg in VP, Dex1, Dex2 and Dex3 groups, and the equal volume of normal saline was given instead in group C. At 15 min be-fore intraperitoneal injection, dexmedetomidine 1, 5 and 10μg∕kg were injected via the tail vein in Dex1, Dex2 and Dex3 groups, respectively, and the equal volume of normal saline was given instead in C and VP groups. Behavioral changes of rats were observed within 60 min after the model was established, and viscer-al pain index ( VPI) was calculated. Blood samples were collected from the hearts at 180 min after establis-hing the model for determination of tumor necrosis factor-alpha ( TNF-α) concentrations in serum. The ani-mals were then sacrificed, and colons were obtained for examination of pathological changes with a light mi-croscope. Results Compared with group C, the VPI and serum TNF-α concentrations were significantly increased in VP and Dex1-2 groups, and the serum TNF-αconcentrations were significantly increased ( P<0. 05), and no significant change was found in VPI in group Dex3 (P>0. 05). Compared with group VP, the VPI and serum TNF-α concentrations were significantly decreased (P<0. 05), and the pathological changes of colon tissues were significantly attenuated in group Dex1-3. Compared with group Dex1, the VPI and serum TNF-α concentrations were significantly decreased ( P<0. 01) , and the pathological changes of colon tissues were significantly attenuated in Dex2-3 groups. Compared with group Dex2, the VPI and ser-um TNF-α concentrations were significantly decreased (P<0. 01), and the pathological changes of colon tissues were significantly attenuated in group Dex3. Conclusion Dexmedetomidine pretreatment can miti-gate inflammatory visceral pain in rats.

Objective To evaluate the effect of intrathecal dexmedetomidine on expression of sub-stance P (SP) and c-fos in the spinal dorsal horns of rats with visceral pain. Methods Thirty-two clean-grade healthy adult male Sprague-Dawley rats, weighing 250-300 g, were divided into 4 groups ( n=8 each) using a random number table method: control group (C group), visceral pain group (VP group), dexmedetomidine group (D group) and dexmedetomidine plus atipamezole group (DA group). VP, D and DA groups received intraperitoneal injection of 0. 9％ acetic acid 10 ml∕kg to establish the model of visceral pain, while group C received the equal volume of normal saline instead. At 10 min before the model was es-tablished, dexmedetomidine 20 μl (1μg∕kg) and dexmedetomidine 1μg∕kg plus atipamezole 1μg∕kg (20μl) were intrathecally injected in D and DA groups, respectively, and the equal volume of normal saline 20μl was given instead in C and VP groups. Visceral pain index ( VPI) was recorded at 1 h after intraperito-neal injection, and then rats were sacrificed, and the dorsal horns of the spinal cord ( L4-6 ) were removed for determination of the expression of SP and c-fos by immunohistochemistry. Results Compared with group C, VPI was significantly increased, and the expression of SP and c-fos was up-regulated in VP, D and DA groups (P<0. 05). Compared with group VP, VPI was significantly decreased, and the expression of SP and c-fos was down-regulated in D and DA groups (P<0. 05). Compared with group D, VPI was signifi-cantly increased, and the expression of SP and c-fos was up-regulated in group DA ( P<0. 05) . Conclusion Intrathecal dexmedetomidine reduces the visceral pain through inhibiting the expression of SP and c-fos in the spinal dorsal horns, which is related to the α2-adrenergic receptor in spinal dorsal horns of rats.

Objective To evaluate the effect of dexmedetomidine on visceral pain in rats and the role of α2 adrenergic receptors in locus coeruleus (LC).Methods Thirty-two healthy adult male SpragueDawley rats,weighing 250-300 g,were divided into 4 groups (n=8 each) using a random number table method:control group (group C),visceral pain group (group VP),dexmedetomidine group (group DEX) and α2-adrenergic receptor antagonist atipamezole group (group AP).α2-adrenergic receptor antagonist atipamezole 522 μg/kg was intramuscularly injected in group AP,and the equal volume of normal saline was given instead in C,VP and DEX groups.At 10 min after intramuscular injection,dexmedetomidine 10 μg/kg was injected via the tail vein in DEX and AP groups,and the equal volume of normal saline was given instead in C and VP groups.VP,DEX and AP groups received intraperitoneal injection of 0.9％ acetic acid 10 ml/kg to make the visceral pain model at 15 min after injection via the tail vein.The cumulative visceral pain score was recorded within 60 min after acetic acid injection.The number of c-fos positive cells in LC was detected by immunohistochemistry,and the content of norepinephrine (NA) in the spinal cord were detected by enzyme-linked immunosorbent assay at 2 h after acetic acid injection.Results Compared with group C,the cumulative visceral pain scores,the number of c-fos positive cells in LC and content of NA in the spinal cord were significantly increased in VP,DEX and AP groups (P＜0.05).Compared with group VP,the cumulative visceral pain scores,the number of c-fos positive cells in LC and content of NA in the spinal cord were significantly decreased in DEX and AP groups (P＜0.05).Compared with group DEX,the cumulative visceral pain scores,the number of c-fos positive cells in LC and content of NA in the spinal cord were significantly increased in group AP (P＜0.05).Conclusion Dexmedetomidine can alleviate visceral pain in rats,and the mechanism is partially related to activating α2 adrenergic receptors in LC.