Biochemical, pathological and ultrastructural investigation of whether lamotrigine has neuroprotective efficacy against spinal cord ischemia reperfusion injury.

INTRODUCTION: Lamotrigine, an anticonvulsant drug with inhibition properties of multi-ion channels, has been shown to be able to attenuates secondary neuronal damage by influencing different pathways. The aim of this study was to look into whether lamotrigine treatment could protect the spinal cord from experimental spinal cord ischemia-reperfusion injury. MATERIALS AND METHODS: Thirty-two rats, eight rats per group, were randomly assigned to the sham group in which only laparotomy was performed, and to the ischemia, methylprednisolone and lamotrigine groups, where the infrarenal aorta was clamped for thirty minutes to induce spinal cord ischemia-reperfusion injury. Tissue samples belonging to spinal cords were harvested from sacrificed animals twenty-four hours after reperfusion. Tumor necrosis factor-alpha levels, interleukin-1 beta levels, nitric oxide levels, superoxide dismutase activity, catalase activity, glutathione peroxidase activity, malondialdehyde levels and caspase-3 activity were studied. Light and electron microscopic evaluations were also performed to reveal the pathological alterations. Basso, Beattie, and Bresnahan locomotor scale and the inclined-plane test was used to evaluate neurofunctional status at the beginning of the study and just before the animals were sacrificed. RESULTS: Lamotrigine treatment provided significant improvement in the neurofunctional status by preventing the increase in cytokine expression, increased lipid peroxidation and oxidative stress, depletion of antioxidant enzymes activity and increased apoptosis, all of which contributing to spinal cord damage through different paths after ischemia reperfusion injury. Furthermore, lamotrigine treatment has shown improved results concerning the histopathological and ultrastructural scores and the functional tests. CONCLUSION: These results proposed that lamotrigine may be a useful therapeutic agent to prevent the neuronal damage developing after spinal cord ischemia-reperfusion injury.

Effects of Ganoderma lucidum Polysaccharides on Different Pathways Involved in the Development of Spinal Cord Ischemia Reperfusion Injury: Biochemical, Histopathologic, and Ultrastructural Analysis in a Rat Model.

OBJECTIVE: Inflammation and oxidative stress are 2 important factors in the emergence of paraplegia associated with spinal cord ischemia-reperfusion injury (SCIRI) after thoracoabdominal aortic surgery. Here it is aimed to investigate the effects of Ganoderma lucidum polysaccharide (GLPS) on SCIRI. METHODS: Rats were randomly selected into 4 groups of 8 animals each: sham, ischemia, methylprednisolone, and GLPS. To research the impacts of various pathways that are efficacious in formation of SCIRI, tumor necrosis factor α, interleukin 1ß, nitric oxide, superoxide dismutase levels, and catalase, glutathione peroxidase activities, malondialdehyde levels, and caspase-3 activity were measured in tissues taken from the spinal cord of rats in all groups killed 24 hours after ischemia reperfusion injury. The Basso, Beattie, and Bresnahan locomotor scale and inclined plane test were used for neurologic assessment before and after SCIRI. In addition, histologic and ultrastructural analyses of tissue samples in all groups were performed. RESULTS: SCIRI also caused marked increase in tissue tumor necrosis factor α, interleukin 1ß, nitric oxide, malondialdehyde levels, and caspase-3 activity, because of inflammation, increased free radical generation, lipid peroxidation, and apoptosis, respectively. On the other hand, SCIRI caused significant reduction in tissue superoxide dismutase, glutathione peroxidase, and catalase activities. Pretreatment with GLPS likewise diminished the level of the spinal cord edema, inflammation, and tissue injury shown by pathologic and ultrastructural examination. Pretreatment with GLPS reversed all these biochemical changes and improved the altered neurologic status. CONCLUSIONS: These outcomes propose that pretreatment with GLPS prevents progression of SCIRI by alleviating inflammation, oxidation, and apoptosis.

Neuroprotective effects of rosuvastatin against traumatic spinal cord injury in rats.

Rosuvastatin, which is a potent statin, has never been studied in traumatic spinal cord injury. The aim of this study was to investigate whether rosuvastatin treatment could protect the spinal cord after experimental spinal cord injury. Rats were randomized into the following five groups of eight animals each: control, sham, trauma, rosuvastatin, and methylprednisolone. In the control group, no surgical intervention was performed. In the sham group, only laminectomy was performed. In all the other groups, the spinal cord trauma model was created by the occlusion of the spinal cord with an aneurysm clip. In the spinal cord tissue, caspase-3 activity, tumor necrosis factor-alpha levels, myeloperoxidase activity, malondialdehyde levels, nitric oxide levels, and superoxide dismutase levels were analyzed. Histopathological and ultrastructural evaluations were also performed. Neurological evaluation was performed using the Basso, Beattie, and Bresnahan locomotor scale and the inclined-plane test.After traumatic spinal cord injury, increases in caspase-3 activity, tumor necrosis factor-alpha levels, myeloperoxidase activity, malondialdehyde levels, and nitric oxide levels were detected. In contrast, the superoxide dismutase levels were decreased. After the administration of rosuvastatin, decreases were observed in the tissue caspase-3 activity, tumor necrosis factor-alpha levels, myeloperoxidase activity, malondialdehyde levels, and nitric oxide levels. In contrast, tissue superoxide dismutase levels were increased. Furthermore, rosuvastatin treatment showed improved results concerning the histopathological scores, the ultrastructural score and the functional tests. Biochemical, histopathological, ultrastructural analysis and functional tests revealed that rosuvastatin exhibits meaningful neuroprotective effects against spinal cord injury.

Efficacy of triage by paramedics: a real-time comparison study.

OBJECTIVES: Triage has evolved as an effective method of separating patients who require immediate medical attention from patients with non-urgent problems. The aim of this study was to assess the agreement between paramedics and emergency residents about triage decisions using the 3-level triage (3L) system and the 5-level (5L) Australian triage scale in real time. METHODS: All patients who presented to a central triage area during a 1-week period were triaged by paramedics and emergency residents. The chance-adjusted measure of agreement kappa (κ) was calculated to evaluate the agreement between triage decisions made by paramedics and by emergency residents. RESULTS: A total of 731 patients were included in the final data analysis. Admitting time and waiting time were significantly consistent in the triage area. Agreement between the triage decisions made by paramedics and by emergency residents was 47% (κ = 0.47) when using the 3L triage scale and 45% (κ = 0.45) when using the 5L triage scale across all cases. A strong correlation existed among the general conditions of the patients, the 3L triage scale, and the 5L triage scale. DISCUSSION: Triaging is commonly performed by nurses in the American emergency system, and triage by paramedics is not common. Few studies are available about triage by paramedics, and more studies are necessary. A new triage scale may be necessary for untrained personnel so that all emergency departments can conduct simple triage.