Propofol has cerebral vascular and metabolic effects similar to those of barbiturates, and it is used to maintain neurosurgical anesthesia because it reduces cerebral metabolic rate, cerebral blood flow, and intracranial pressure. Although the use of propofol as a cerebral protectant during certain neurosurgical procedures has been advocated, consensus has not been reached as to a protective effect of propofol on cerebral ischemia. In this study we observed the neuroprotective effects of propofol during global cerebral ischemia-reperfusion injury by the use of four-vessel occlusion method in a rat model. We measured the levels of malondialdehyde as a marker of lipid peroxidation in ischemic tissue, and the results indicate that propofol plays a role in the inhibition of neuronal death induced by brain ischemia.
Traumatic injury to central nervous system results in the production of inflammatory cytokines via intrinsic mechanisms by neurons, astrocytes and microglia, and extrinsic mechanisms by infiltrating macrophages, lymphocytes and other leukocytes. Interleukin-1 beta is the key mediator of the acute inflammatory host response. While this response is necessary for resolution of the pathologic event, the toxic nature of many of its products can cause significant tissue damage. We analyzed serum interleukin-1 beta levels by enzyme-linked immunosorbent assay in 48 patients with solitary head injury who were transported to our clinic immediately after trauma. We categorized the patients according to their initial Glasgow coma scores in three groups, and compared their serum interleukin-1 beta values both with their Glasgow coma initial and outcome scores. This study helped to provide quantitative data to estimate clinical impressions and prognosis after head injury.
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