D K Resnick1, P Nguyen, C F Cechvala. 1. Department of Neurological Surgery, University of Wisconsin School of Medicine, K4/834 Clinical Science Center, 600 Highland Avenue, Madison, WI 53792, USA. Resnick@neurosurg.wisc.edu
Abstract
BACKGROUND CONTEXT: Inflammatory metabolites of arachidonic acid likely play a significant role in secondary injury after spinal cord trauma. PURPOSE: We sought to characterize the regional and temporal alterations in prostaglandin concentrations after injury in a rat model. STUDY DESIGN/ SETTING: Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) concentrations were measured in cerebrospinal fluid (CSF) and in different parts of the injured spinal cord at various time points after spinal cord injury. OUTCOME MEASURES: PGE2 and TxB2 levels were measured by means of an enzyme immune assay. METHODS: Forty-six adult Long Evans rats were subject to spinal cord injury using the NYU impactor. Animals were divided into three groups. Fourteen animals were used in a pilot study to determine the timing and location of PGE2 production after spinal cord injury. These animals were sacrificed, and samples of injured cord, rostral cord and CSF were assayed for PGE2 concentration. The remaining 32 animals were used to establish the time course of prostaglandin production. Twenty-eight animals were subjected to a spinal cord injury, and four animals served as sham-operated controls. These animals were sacrificed at predetermined time points 2 to 72 hours after injury, and the injured segments of spinal cord were harvested. RESULTS: Both PGE2 and TxB2 concentrations increased immediately after injury in the injured segment. PGE2 concentrations increased faster and more dramatically in the injured segment of spinal cord than in CSF or noninjured segments. Elevations in PGE2 and TxB2 concentrations were persistent for 72 hours after injury. CONCLUSION: Elevated concentrations of arachidonic acid metabolites can be detected in the injured segment of the spinal cord for at least 72 hours after injury. Concentration changes are detected earlier and are more dramatic in the injured cord segment than in rostral segments or the CSF.
BACKGROUND CONTEXT: Inflammatory metabolites of arachidonic acid likely play a significant role in secondary injury after spinal cord trauma. PURPOSE: We sought to characterize the regional and temporal alterations in prostaglandin concentrations after injury in a rat model. STUDY DESIGN/ SETTING:Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) concentrations were measured in cerebrospinal fluid (CSF) and in different parts of the injured spinal cord at various time points after spinal cord injury. OUTCOME MEASURES: PGE2 and TxB2 levels were measured by means of an enzyme immune assay. METHODS: Forty-six adult Long Evans rats were subject to spinal cord injury using the NYU impactor. Animals were divided into three groups. Fourteen animals were used in a pilot study to determine the timing and location of PGE2 production after spinal cord injury. These animals were sacrificed, and samples of injured cord, rostral cord and CSF were assayed for PGE2 concentration. The remaining 32 animals were used to establish the time course of prostaglandin production. Twenty-eight animals were subjected to a spinal cord injury, and four animals served as sham-operated controls. These animals were sacrificed at predetermined time points 2 to 72 hours after injury, and the injured segments of spinal cord were harvested. RESULTS: Both PGE2 and TxB2 concentrations increased immediately after injury in the injured segment. PGE2 concentrations increased faster and more dramatically in the injured segment of spinal cord than in CSF or noninjured segments. Elevations in PGE2 and TxB2 concentrations were persistent for 72 hours after injury. CONCLUSION: Elevated concentrations of arachidonic acid metabolites can be detected in the injured segment of the spinal cord for at least 72 hours after injury. Concentration changes are detected earlier and are more dramatic in the injured cord segment than in rostral segments or the CSF.
Authors: M Lanza; M Campolo; G Casili; A Filippone; I Paterniti; S Cuzzocrea; Emanuela Esposito Journal: Mol Neurobiol Date: 2018-09-18 Impact factor: 5.590
Authors: Nai-Kui Liu; Ling-Xiao Deng; Yi Ping Zhang; Qing-Bo Lu; Xiao-Fei Wang; Jian-Guo Hu; Eddie Oakes; Joseph V Bonventre; Christopher B Shields; Xiao-Ming Xu Journal: Ann Neurol Date: 2014-04-02 Impact factor: 10.422