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.
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ABSTRACT: We evaluated the effects of dexmedetomidine pretreatment on bupivacaine cardiotoxicity in anesthetized rats. Sixteen Wistar-Albino male rats (300-400 g) were anesthetized with ketamine. Electrocardiographic and invasive blood pressure monitoring were performed, and the results were continuously recorded. The rats were randomized into 2 groups. In group D, rats were pretreated with intravenous dexmedetomidine at a dose of 10 Kg/kg (n = 8), whereas in group S, rats were pretreated with intravenous saline (n = 8). Fifteen minutes later, bupivacaine was infused at a rate of 3 mg/kg per minute until cardiac asystole occurred. The timing of specific cardiotoxic events (a 25%, 50%, and 75% reductions of mean arterial pressure and heart rate as well as occurrence of the first arrhythmia and asystole) was recorded. Dexmedetomidine pretreatment reduced the heart rates and mean arterial pressures of the rats who received it (P G 0.05). Dexmedetomidine pretreatment before bupivacaine administration also significantly increased the time to the 25%, 50%, and 75% reductions in mean arterial pressure and the time to the 25% and 50% reductions in heart rate (P G 0.05). In addition, dexmedetomidine significantly increased the time to first arrhythmia and time to asystole (P G 0.05) in the rats who received it before receiving bupivacaine. Dexmedetomidine pretreatment delays the effects of bupivacaine cardiotoxicity.Regional anesthesia and pain medicine 01/2009; 34(6):565-8. DOI:10.1097/AAP.0b013e3181bfbe35 · 2.12 Impact Factor
Conference Paper: Solving the problem of heating of RF contacts in cavity tuners[Show abstract] [Hide abstract]
ABSTRACT: The accelerating cavity of the ASTRID Electron Synchrotron was studied. The cavity is a capacity loaded TEM cavity resonating at 104.95 MHz. Two plungers driven in parallel keep the cavity in tune, yielding a tuning range of about 0.8 MHz to compensate the beam loading. The RF spring contact liners placed on the entrance of the plunger housing are used to isolate the plunger housing from the RF field. The surface current flowing through the contacts limits the power in the cavity to less than 5 kW due to heating. We analyse the electrodynamics of the tuner and investigate two options of a new tuner geometry, one with contacts and one without contacts. The new design should remove the power limitation due to contact problemsParticle Accelerator Conference, 1997. Proceedings of the 1997; 06/1997
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ABSTRACT: The present study aimed to investigate the neuroprotective efficacy of dexmedetomidine in a rat experimental spinal cord injury model. The rats (n=40) were equally divided into four groups: G1, G2, G3, and G4. Rats in the G1 group underwent a laminectomy only. For the rats in the G2, G3, and G4 groups, spinal cord injury was induced by placing an aneurysm clip extradurally for 60 s at T10. The rats in G2 did not receive any post-injury treatment. Immediately after trauma was induced, rats in G3 were given methylprednisolone (30 mg/kg) and in G4, dexmedetomidine (10 microg/kg), both intraperitoneally. The rats were sacrificed under anesthesia 24 hours later and 1.5 cm lengths of injured spinal cord were obtained. Malonyldialdehyde values were significantly increased in G2 compared to G1, G3 and G4 (p<0.05). The neuronal cell count in G1 was significantly higher than in G2 and G3 (p=0.0001; p=0.007). G4 had higher cell counts compared to G2 and G3 (p=0.0001; p=0.05). These findings indicated that dexmedetomidine might have neuroprotective effects in spinal cord injury.Journal of Clinical Neuroscience 04/2010; 17(4):490-4. DOI:10.1016/j.jocn.2009.05.041 · 1.32 Impact Factor