کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11025562 | 1678522 | 2019 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Engaging pain fibers after a spinal cord injury fosters hemorrhage and expands the area of secondary injury
ترجمه فارسی عنوان
پیوند الیاف درد بعد از آسیب نخاعی موجب خونریزی و گسترش ناحیه آسیب ثانویه می شود
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کلمات کلیدی
BSCBTNFTRPM4PolytraumaPHNIL-18IL-1ßTBSTECLANCOVATRPV1PVDFH&E - H & ESUR1 - sur1Secondary injury - آسیب دومSpinal cord injury - آسیب نخاعیElectrochemiluminescence - الکتروکمی لومینسانسInterleukin-18 - اینترلوکین ۱۸interleukin-1ß - اینترلوکین-1ßanalysis of covariance - تجزیه و تحلیل کوواریانسanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceTris-buffered saline Tween-20 - تریس بافر Tween-20 سالینHemorrhage - خونریزیPain - دردpolyvinylidene difluoride - دی فلوئورید پلی وینیلیدینBBB - سد خونی مغزیsci - علمیnociception - غربالگریtumor necrosis factor - فاکتور نکروز تومورThoracic - قفسه سینهBlood-spinal cord barrier - مانع خون بند نافBlood spinal cord barrier - مانع طناب نخاعی خونHematoxylin & Eosin - هماتوکسیلین و ائوزینtransient receptor potential cation channel subfamily V member 1 - کانال زیر کانال کانتینت گیرنده گذرا V عضو 1sulfonylurea receptor 1 - گیرنده سولفونیل اوره 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
چکیده انگلیسی
In humans, spinal cord injury (SCI) is often accompanied by additional tissue damage (polytrauma) that can engage pain (nociceptive) fibers. Prior work has shown that this nociceptive input can expand the area of tissue damage (secondary injury), undermine behavioral recovery, and enhance the development of chronic pain. Here, it is shown that nociceptive input given a day after a lower thoracic contusion injury in rats enhances the infiltration of red blood cells at the site of injury, producing an area of hemorrhage that expands secondary injury. Peripheral nociceptive fibers were engaged 24â¯h after injury by means of electrical stimulation (shock) applied at an intensity that engages unmyelinated pain (C) fibers or through the application of the irritant capsaicin. Convergent western immunoblot and cyanmethemoglobin colorimetric assays showed that both forms of stimulation increased the concentration of hemoglobin at the site of injury, with a robust effect observed 3-24â¯h after stimulation. Histopathology confirmed that shock treatment increased the area of hemorrhage and the infiltration of red blood cells. SCI can lead to hemorrhage by engaging the sulfonylurea receptor 1 (SUR1) transient receptor potential melastatin 4 (TRPM4) channel complex in neurovascular endothelial cells, which leads to cell death and capillary fragmentation. Histopathology confirmed that areas of hemorrhage showed capillary fragmentation. Co-immunoprecipitation of the SUR1-TRPM4 complex showed that it was up-regulated by noxious stimulation. Shock-induced hemorrhage was associated with an acute disruption in locomotor performance. These results imply that noxious stimulation impairs long-term recovery because it amplifies the breakdown of the blood spinal cord barrier (BSCB) and the infiltration of red blood cells, which expands the area of secondary injury.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 311, January 2019, Pages 115-124
Journal: Experimental Neurology - Volume 311, January 2019, Pages 115-124
نویسندگان
Joel D. Turtle, Melissa K. Henwood, Misty M. Strain, Yung-Jen Huang, Rajesh C. Miranda, James W. Grau,