Effects of dexmedetomidine or methylprednisolone on inflammatory responses in spinal cord injury
ABSTRACT The aim of this study was to compare the anti-inflammatory response of methylprednisolone and the alpha2-agonist dexmedetomidine in spinal cord injury (SCI).
Twenty-four male adult Wistar albino rats, weight 200-250 g, were included in the study. The rats were divided into four groups as follows: the control group (n: 6) received only laminectomy; the SCI group (n: 6) with trauma alone; the SCI+methylprednisolone group (n: 6) with trauma and 30 mg/kg methylprednisolone, followed by a maintenance dose of 5.4 mg/kg/h; and the SCI+dexmedetomidine group (n: 6) with trauma and 10 microg/kg dexmedetomidine treatment intraperitoneally. Twenty-four hours after the trauma, spinal cord samples were taken for histopathological examination and serum samples were collected for interleukin-6 (IL-6) and tumor necrosis factor (TNF)-alpha measurement.
TNF-alpha (P=0.009) and IL-6 (P=0.009) levels were significantly increased in the SCI group. TNF-alpha and IL-6 levels were significantly decreased with methylprednisolone (P=0.002, 0.002) and dexmedetomidine (P=0.002, 0.009) treatment, respectively. Methylprednisolone and dexmedetomidine treatment reduced neutrophils' infiltration in SCI.
The current study does not clarify the definitive mechanism by which dexmedetomidine decreases inflammatory cytokines but it is the first study to report the anti-inflammatory effect of dexmedetomidine in SCI. Further studies are required to elucidate the effects of dexmedetomidine on the inflammatory response.
[Show abstract] [Hide abstract]
ABSTRACT: To determine whether postoperative cardiac surgery patients who are sedated with dexmedetomidine have fewer atrial arrhythmias, and whether dexmedetomidine is associated with fewer renal and more gastrointestinal (GI) complications. Retrospective study. Urban academic hospital. The records of 765 postoperative cardiac surgery patients who were given dexmedetomidine for postoperative sedation in the intensive care unit (ICU) were studied. Data from the hospital's Cardiac Anesthesiology database between the years 2005 and 2010 were evaluated. Records of patients whose ASA physical status was > 4 or who were < 18 years of age were excluded from the study. Patients who were and were not given dexmedetomidine were compared for postoperative sedation within three days after cardiac surgery using multivariable logistic regression, adjusting for imbalanced covariables. The records of 17,776 patients, including 765 cardiac patients given dexmedetomidine for postoperative sedation in the ICU, were reviewed. Patients who received postoperative dexmedetomidine had a lower risk of having atrial arrhythmias: (OR 0.74 (95% CI: 0.60, 0.91; P = 0.004). Dexmedetomidine was not associated with 30-day mortality (1.10, 0.40 - 3.02; P = 0.86), or with any of the following 30-day outcomes: surgical infection (0.72, 0.36-1.42; P = 0.34), systemic infection (1.38, 0.93 - 2.05; P = 0.11), GI complications (1.34, 0.74 - 2.42; P = 0.33), or renal complications (1.23, 0.70 - 2.15; P = 0.48). Dexmedetomidine use after cardiac surgery was associated with a lower incidence of atrial arrhythmias. Copyright © 2014 Elsevier Inc. All rights reserved.Journal of Clinical Anesthesia 10/2014; DOI:10.1016/j.jclinane.2014.05.009 · 1.21 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: To explore the effect of dexmedetomidine (DEX) post-treatment on the inflammatory response of astrocyte induced by lipopolysaccharide (LPS). The astrocytes of neonatal mice were primarily cultured in vitro. After purification and identification, the cells were divided into five groups: group C: control group; group L: astrocytes were treated with 1 μg/ml LPS for 24 h; group D1, D2, and D3: astrocytes were pretreated with 1 μg/ml for 24 h LPS, and then cultured with low (0.1 μM), medium (1 μM), high (10 μM) concentration of DEX for 30 min, respectively. The cell survival rate was detected by cell counting kit. The expressions of inducible nitric oxide synthase (iNOS) mRNA, tumor necrosis gactor-α (TNF-α) mRNA, and interleukin-1β (IL-1β) mRNA were measured by RT-PCR in cell lysis solution of every group. The concentration of nitric oxide (NO) was detected by Griess method. The concentrations of IL-1β and TNF-α were measured, respectively, by enzyme-linked immuno sorbent assay. Compared with the group C, the expressions of iNOS mRNA, TNF-α mRNA, and IL-1βm RNA were significantly up-regulated, the release of NO, TNF-α, and IL-1β was significantly increased in group L (P < 0.05). Compared with group L, mRNA levels of inflammation-related factors and release of inflammatory factors were significantly down-regulated in group D2 and D3 (P < 0.05). There was no statistical difference between group D1 and group L. Pre-treatment with medium and high concentration of DEX can inhibit the LPS-induced inflammatory response of astrocyte.Cell Biochemistry and Biophysics 10/2014; 71(1). DOI:10.1007/s12013-014-0213-0 · 2.38 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: The aim of this study was to examine whether dexmedetomidine improves acute liver injury in a rat model. Twenty-eight male Wistar albino rats weighing 300-350 g were allocated randomly to four groups. In group 1, normal saline (NS) was injected into the lungs and rats were allowed to breathe spontaneously. In group 2, rats received standard ventilation (SV) in addition to NS. In group 3, hydrochloric acid was injected into the lungs and rats received SV. In group 4, rats received SV and 100 µg/kg intraperitoneal dexmedetomidine before intratracheal HCl instillation. Blood samples and liver tissue specimens were examined by biochemical, histopathological, and immunohistochemical methods. Acute lung injury (ALI) was found to be associated with increased malondialdehyde (MDA), total oxidant activity (TOA), oxidative stress index (OSI), and decreased total antioxidant capacity (TAC). Significantly decreased MDA, TOA, and OSI levels and significantly increased TAC levels were found with dexmedetomidine injection in group 4 (P < 0.05). The highest histologic injury scores were detected in group 3. Enhanced hepatic vascular endothelial growth factor (VEGF) expression and reduced CD68 expression were found in dexmedetomidine group compared with the group 3. In conclusion, the presented data provide the first evidence that dexmedetomidine has a protective effect on experimental liver injury induced by ALI.BioMed Research International 08/2014; 2014:621827. DOI:10.1155/2014/621827 · 2.71 Impact Factor