Early Surgical Decompression Restores Neurovascular Blood Flow and Ischemic Parameters in an in Vivo Animal Model of Nerve Compression Injury.

摘要: Background: Chronic nerve compression neuropathies result in decreased blood flow at the site of compression. Surgical decompression often has variable postoperative results. The current study examines whether timing surgical intervention is an important reversing compression-induced ischemia and associated changes biochemical markers. Methods: An established model chronic injury was created 100 C57BL/6 mice, serial electrophysiological examinations were used to confirm creation a injury. Laser speckle imaging measure neural flow. Nerves animals that did not undergo harvested two, four, six weeks after analyzed for hypoxia-inducible factor 1α (HIF1α), catalase, superoxide dismutase (SOD), matrix metalloproteinases (MMPs) 2 9. other performed either early (two-week) or late (six-week) time point injury, with specimens multiple points decompression. One-way analysis variance Bonferroni correction performed. Results: initially induced hyperemia (1.37 ± 0.50 times contralateral, uninjured nerve) followed by decline four (0.66 0.14, p = 0.0313). In parallel, HIF1α, SOD elevated compression, whereas extracellular matrix-altering proteins later disease. Although yielded return hyperemic state (1.35 0.16, 0.0057), reversal abnormal neurovascular With decompression, MMP9-mediated structural alteration seen, producing irreversible parameters. conduction velocity measurements returned normal two irrespective intervention, distal latency only (0.97 0.06 msec compared 1.22 0.009). Conclusions: injuries upregulating MMP9. Early offered better parameters intervention. Clinical Relevance: These data present clinical correlate functional outcomes seen following release provide support using as predictor release.