Mechanisms underlying alterations in somatosensation and excercise induced pain following ischemic injury

缺血性损伤导致躯体感觉的变化和增强的运动引起的疼痛。在后爪缺血再灌注损伤后，大鼠表现出对机械刺激的缩爪阈值降低，表明运动是疼痛的行为，并且它们在运动后表现出甚至更低的缩爪阈值。为了阐明这些改变的潜在机制，我们将比较运动对未处理大鼠和后爪IR损伤大鼠的影响：1）使用激光多普勒血流仪和组织氧分压测量的后爪肌肉温度调节和营养血流量; 2）使用印度墨水灌注和线粒体氧化能力测量的后爪肌肉毛细血管无复流和肌肉损伤; 3）使用比色测定和组织pH评估的后爪肌肉乳酸盐产生和组织酸中毒; 4）非选择性和选择性ASIC拮抗剂在具有缺血-再灌注损伤的大鼠中的抗伤害感受作用。

Ischemic injury leads to changes in somatosensory perception and enhanced exercise-induced pain. After ischemia-reperfusion injury in the hind paw, rats exhibit lowered paw-withdrawal thresholds to mechanical stimulation, behaviours suggesting that exercise is painful, and they exhibit even lower paw-withdrawal thresholds after exercise. To address the mechanisms underlying these alterations, we will compare the effects of exercise in naïve rats and rats with a hind paw IR injury on: 1) hind paw muscle thermoregulatory and nutritive blood flow using laser Doppler flowmetry and measures of tissue oxygen partial pressure; 2) hind paw muscle capillary no-reflow and muscle injury using India ink perfusion and a measure of mitochondrial oxidative capacity; 3) hind paw muscle lactate production and tissue acidosis using colorometric assays and assessment of tissue pH; 4) the antinociceptive effects of non-selective and selective ASIC antagonists in rats with ischemia-reperfusion injury.