***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    ***EXAMPLES*** 
    Input: We have compared the effects of dexmedetomidine and propofol on endocrine , metabolic , inflammatory and cardiovascular responses in patients in the intensive care unit ( ICU ) after major surgery . Twenty patients who were expected to require 8 h of post-operative sedation and ventilation were allocated r and omly to receive either an infusion of dexmedetomidine 0.2 - 2.5 microg kg(-1 ) h(-1 ) or propofol 1 - 3 mg kg(-1 ) h(-1 ) . Arterial pressure , heart rate and sequential concentrations of circulating cortisol , adrenocorticotrophic hormone ( ACTH ) , growth hormone , prolactin , insulin , glucose and interleukin 6 were measured . An ACTH stimulation test was performed in all patients who received dexmedetomidine .  Heart rate was significantly lower in the dexmedetomidine patients . There were no differences in arterial pressure , cortisol , ACTH , prolactin and glucose concentrations between the two groups . A positive response to the ACTH stimulation test varied depending on the diagnostic criteria used . The insulin concentration was significantly lower in the dexmedetomidine group at 2 h ( P=0.021 ) , although this did not affect blood glucose concentrations . Growth hormone concentrations were significantly higher in dexmedetomidine-treated patients overall ( P=0.036 ) , but circulating concentrations remained in the physiological range . Interleukin 6 decreased in the dexmedetomidine group . We conclude that dexmedetomidine infusion does not inhibit adrenal steroidogenesis when used for short-term sedation after surgery Introduction Sepsis , a systemic inflammatory response to infective etiologies , has a high mortality rate that is linked both to excess cytokine activity and apoptosis of critical immune cells . Dexmedetomidine has recently been shown to improve outcome in a septic cohort of patients when compared to patients r and omized to a benzodiazepine-based sedative regimen . We sought to compare the effects of dexmedetomidine and midazolam , at equi-sedative doses , on inflammation and apoptosis in an animal model of severe sepsis . Methods After central venous access , Sprague Dawley rats underwent cecal ligation and intestinal puncture ( CLIP ) with an 18 G needle without antibiotic cover and received either saline , or an infusion of comparable volume of saline containing midazolam ( 0.6 mg.kg-1.h-1 ) or dexmedetomidine ( 5 ug.kg-1.h-1 ) for 8 hours . Following baseline measurements and CLIP , blood was sample d for cytokine measurement ( tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 ; n = 4 - 6 per group ) at 2 , 4 and 5 hours , and animal mortality rate ( MR ) was monitored ( n = 10 per group ) every 2 hours until 2 hours had elapsed . In addition , spleens were harvested and apoptosis was assessed by immunoblotting ( n = 4 per group ) . Results The 24 hour MR in CLIP animals ( 90 % ) was significantly reduced by sedative doses of either dexmedetomidine ( MR = 20 % ) or midazolam ( MR = 30 % ) . While both sedatives reduced systemic levels of the inflammatory cytokine TNF-alpha ( P < 0.05 ) ; only dexmedetomidine reduced the IL-6 response to CLIP , though this narrowly missed achieving significance ( P = 0.05 ) . Dexmedetomidine reduced splenic caspase-3 expression ( P < 0.05 ) , a marker of apoptosis , when compared to either midazolam or saline . Conclusions Sedation with midazolam and dexmedetomidine both improve outcome in polymicrobial severely septic rats . Possible benefits conveyed by one sedative regimen over another may become evident over a more prolonged time-course as both IL-6 and apoptosis were reduced by dexmedetomidine but not midazolam . Further studies are required to evaluate this hypothesis Background Some studies have demonstrated dexmedetomidine has anti-inflammatory effect on septic rats . However , the mechanism of how dexmedetomidine exerts these effects is still remained unknown . This study was design ed to investigate the mechanism of how dexmedetomidine inhibits the production of inflammatory mediators in cecal ligation and puncturinduced septic rats . Methods 48 Sprague-Dawley rats were r and omly divided into six groups : sham-operated ( sham ) group , cecal ligation and puncture ( CLP ) group , dexmedetomidine 5 μg/kg ( DEX5 ) group , dexmedetomidine 10 μg/kg ( DEX10 ) group , dexmedetomidine + yohimbine ( DEX10 + Yoh ) group and yohimibine group ( Yoh ) . Blood , bronchoalveolarlavage fluid ( BALF ) and lung tissues in each group were collected at six hours after dexmedetomidine or yohimbine treatment , . Tumor necrosis factor-α ( TNF-α ) and interleukin-6 ( IL-6 ) in BALF and plasma were measured by enzyme-linked immunosorbent assay ( ELISA ) . Toll-like receptor-4(TLR4 ) and myeloid differerntiation factor(MyD88 ) expression were measuredby quantitative PCR , and extracellular signal-regulated kinase ( ERK ) 1/2 phosphorylation were determined by western blott . Results Compared with CLP group , dexmedetomidine significantly decreased not only the production of TNF-α and IL-6 both in plasma and BALF , but also inhibited the expression of TLR4 and MyD88 in mRNA level and the activation of ERK1/2 and NF-κB in the lung tissues of CLP-induced septic rats . All these effects could not be reversed by yohimibine . Conclusions Dexmedetomidine treatment can effectively reduce the generation of inflammatory mediators in the plasma and BALF of CLP-induced septic rats . These effects of dexmedetomidine rely on TLR4/MyD88/MAPK/ NF-κB signaling pathway and are independent of α2-adrenoceptor Rationale : Dexmedetomidine is associated with less delirium than benzodiazepines and better sleep architecture than either benzodiazepines or propofol ; its effect on delirium and sleep when administered at night to patients requiring sedation remains unclear . Objectives : To determine if nocturnal dexmedetomidine prevents delirium and improves sleep in critically ill adults . Methods : This two‐center , double‐blind , placebo‐controlled trial r and omized 100 delirium‐free critically ill adults receiving sedatives to receive nocturnal ( 9:30 p.m. to 6:15 a.m. )  intravenous dexmedetomidine ( 0.2 & mgr;g/kg/h , titrated by 0.1 & mgr;g /kg/h every 15 min until a goal Richmond Agitation and Sedation Scale score of −1 or maximum rate of 0.7 & mgr;g/kg/h was reached ) or placebo until ICU discharge . During study infusions , all sedatives were halved ; opioids were unchanged . Delirium was assessed using the Intensive Care Delirium Screening Checklist every 12 hours throughout the ICU admission . Sleep was evaluated each morning by the Leeds Sleep Evaluation Question naire . Measurements and Main Results : Nocturnal dexmedetomidine ( vs. placebo ) was associated with a greater proportion of patients who remained delirium‐free  during the ICU stay ( dexmedetomidine [ 40 ( 80 % ) of 50 patients ] vs. placebo [ 27 ( 54 % ) of 50 patients ] ; relative risk , 0.44 ; 95 % confidence interval , 0.23‐0.82 ; P = 0.006 ) . The average Leeds Sleep Evaluation Question naire score was similar ( mean difference , 0.02 ; 95 % confidence interval , 0.42‐1.92 ) between the 34 dexmedetomidine ( average seven assessment s per patient ) and 30 placebo ( six per patient ) group patients able to provide one or more assessment s. Incidence of hypotension , bradycardia , or both did not differ significantly between groups . Conclusions : Nocturnal administration of low‐dose dexmedetomidine in critically ill adults reduces the incidence of delirium during the ICU stay ; patient‐reported sleep quality appears unchanged . Clinical trial registered with www . clinical trials.gov ( NCT01791296 ) The aim was to verify that dexmedetomidine ( DEX ) can attenuate CLP-induced intestinal injury via inhibition of inflammation . Male Sprague-Dawley ( SD ) rats were r and omly allocated into Sham group and the other three CLP model groups , in terms of different treatments : placebo , DEX , and yohimbine plus DEX ( DEX + YOH ) groups  . Pathology examination was conducted with HE stain . To identify differences among groups , the levels of DAO , and D-lactate in serum were measured by spectrophotometry , and the levels of TNF-α , IL-1β , and IL-6 in serum and organ were measured by ELISA . The expressions of occludin and TLR4 in tissue were detected by Western blot . The survival rate of an additional group of animals within 7 d was recorded . In DEX group , mortality was lower , histology change was minor , DAO , and D-lactate levels were reduced , and occludin expression was increased ; the expressions of TNF-α , IL-1β , IL-6 , and TLR4 were also decreased in DEX group . These results indicated that acute intestinal injury induced by CLP was mitigated by DEX treatment . However , these effects of DEX were significantly attenuated by yohimbine in DEX + YOH group . Our study indicated the protective effects of DEX on CLP-induced injury , which may be associated with the inhibition of inflammation via modulating TLR4 pathway and can be blocked by yohimbine Background : Dexmedetomidine , an & agr;-2 adrenergic receptor agonist , has already been used in septic patients although few studies have examined its effects on microcirculatory dysfunction , which may play an important role in perpetuating sepsis syndrome . Therefore , the authors have design ed a controlled experimental study to characterize the microcirculatory effects of dexmedetomidine in an endotoxemia rodent model that allows in vivo studies of microcirculation . Methods : After skinfold chamber implantation , 49 golden Syrian hamsters were r and omly allocated in five groups : ( 1 ) control animals ; ( 2 ) nonendotoxemic animals treated with saline ; ( 3 ) nonendotoxemic animals treated with dexmedetomidine ( 5.0 & mgr;g kg−1 h−1 ) ; ( 4 )  endotoxemic ( lipopolysaccharide 1.0 mg/kg ) animals treated with saline ; and ( 5 ) endotoxemic animals treated with dexmedetomidine . Intravital microscopy of skinfold chamber preparations allowed quantitative analysis of microvascular variables and venular leukocyte rolling and adhesion . Mean arterial blood pressure , heart rate , arterial blood gases , and lactate concentrations were also documented . Results : Lipopolysaccharide administration increased leukocyte rolling and adhesion and decreased capillary perfusion .  Dexmedetomidine significantly attenuated these responses : compared with endotoxemic animals treated with saline , those treated with dexmedetomidine had less leukocyte rolling ( 11.8 ± 7.2 % vs. 24.3 ± 15.0 % ; P < 0.05 ) and adhesion ( 237 ± 185 vs. 510 ± 363 ; P < 0.05 ) and greater functional capillary density ( 57.4 ± 11.2 % of baseline values vs. 45.9 ± 11.2 % ; P < 0.05 ) and erythrocyte velocity ( 68.7 ± 17.6 % of baseline values vs. 54.4 ± 14.8 % ; P < 0.05 ) at the end of the experiment . Conclusions : Dexmedetomidine  decreased lipopolysaccharide-induced leukocyte – endothelial interactions in the hamster skinfold chamber microcirculation . This was accompanied by a significant attenuation of capillary perfusion deficits , suggesting that dexmedetomidine yields beneficial effects on endotoxemic animals ’ microcirculation BACKGROUND Dexmedetomidine reduced mortality and inhibited the inflammatory response  during endotoxemia in rats . The aim of this study was to clarify the effect of dexmedetomidine-regulating inflammation on a noninfectious , ventilator-induced lung injury ( VILI ) in dogs . METHODS Thirty healthy Beagles weighing between 8 and 12 kg were r and omly divided into five groups : control group ( group C , n = 6 ) , mechanical ventilation ( group MV , n = 6 ) , and three different doses of dexmedetomidine group ( group DEX1 - 3 , n = 6 ) . 
    Output:
    
Conclusion Evidence supports potential anti-inflammatory effects from α2 agonists , but the relevance to clinical ly important outcomes is uncertain .