Can M, Gul S, Bektas S, Hanci V, Acikgoz S: Effects of dexmedetomidine or methylprednisolone on inflammatory responses in spinal cord injury

Department of Biochemistry, Faculty of Medicine, Karaelmas University, Zonguldak, Turkey.
Acta Anaesthesiologica Scandinavica (Impact Factor: 2.32). 07/2009; 53(8):1068-72. DOI: 10.1111/j.1399-6576.2009.02019.x
Source: PubMed


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.

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    • "The protective effects of dexmedetomidine in the lungs have been demonstrated in previous studies [21, 22]; however, the effect of dexmedetomidine in the protection against liver injury is not clear. Previously it has been reported that dexmedetomidine has a potent anti-inflammatory capacity [21, 22, 27, 36]. The experimental studies showed that dexmedetomidine attenuates interleukin-6 and tumor necrosis factor-α levels [36]. "
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    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 · 1.58 Impact Factor
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    • "To date, the mechanism underlying the role of DEX in the reduction of cytokine secretion is still a matter of debate. One group reported that DEX administration led to a reduced inflammatory response during the treatment of spinal cord injury, confirming the anti-inflammatory effects of DEX [28]. Another group reported that DEX protected nerve tissue from reperfusion-induced injury after -erm brain ischemia via reduced levels of TNF-α and decreased numbers of degenerative neurons in the hippocampus and dentate gyrus [29]. "
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    ABSTRACT: Dexmedetomidine (DEX) is an α 2-adrenergic agonist. It decreases the levels of norepinephrine release, resulting in a reduction of postsynaptic adrenergic activity. In the present study, the effects of DEX on postpartum bleeding-induced multiple organ dysfunction syndrome (BMODS) were studied in rats in which BMODS was induced by the combination of hypotension and clamping of the superior mesenteric artery. We evaluated the role of dexmedetomidine (DEX) in cytokine release during postpartum BMODS in rats. In summary, the present study demonstrated that DEX administration reduced IFN-r and IL-4 release and decreased lung injury during postpartum BMODS. It is possible that DEX administration decreased inflammatory cytokine production in BMODS by inhibiting inflammation and free radical release by leukocytes independent of the DEX dose.
    Mediators of Inflammation 06/2013; 2013(2):627831. DOI:10.1155/2013/627831 · 3.24 Impact Factor
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    • "Meanwhile, the intraperitoneal administration of dexmedetomidine in a spinal cord injury model of rat had significantly reduced the level of tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6 which increased after spinal cord injury (19). Besides, the administration of dexmedetomidine reduced the levels of TNF-α, IL-1, and IL-6 in patients with severe septic manifestation subsequent to the ileus surgery (20). "
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    ABSTRACT: Dexmedetomidine, which is a selective α2-adrenoceptor agonist, was recently introduced into clinical practice for its analgesic properties. The purpose of this study was to evaluate the effects of dexmedetomidine in a vincristine-evoked neuropathic rat models. Sprague-Dawley rats were injected intraperitoneally with vincristine or saline (0.1 mg/kg/day) using a 5-day-on, 2-day-off schedule for 2 weeks. Saline and dexmedetomidine (12.5, 25, 50, and 100 µg/kg) were injected to rats developed allodynia 14 days after vincristine injection, respectively. We evaluated allodynia at before, 15, 30, 60, 90, 120, 180, and 240 min, and 24 hr after intraperitoneal drug (normal saline or dexmedetomidine) injection. Saline treatment did not show any differences for all the allodynia. Maximal paw withdrawal thresholds to mechanical stimuli were 3.0 ± 0.4, 9.1 ± 1.9, 13.0 ± 3.6, 16.6 ± 2.4, and 24.4 ± 1.6 g at saline, 12.5, 25, 50, and 100 µg/kg dexmedetomidine injection, respectively. Minimal withdrawal frequency to cold stimuli were 73.3 ± 4.2, 57.1 ± 6.8, 34.3 ± 5.7, 20.0 ± 6.2, and 14.3 ± 9.5 g at saline, 12.5, 25, 50, and 100 µg/kg dexmedetomidine injection, respectively. Dexmedetomidine shows a dose-dependent antiallodynic effect on mechanical and cold stimuli in vincristine-evoked neuropathic rat models (P < 0.05).
    Journal of Korean medical science 11/2012; 27(11):1411-7. DOI:10.3346/jkms.2012.27.11.1411 · 1.27 Impact Factor
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