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

缺血性损伤导致躯体感觉的改变和运动性疼痛的增加。后爪缺血再灌注损伤后，大鼠对机械刺激的缩爪阈值降低，这表明运动是痛苦的，运动后的缩爪阈值甚至更低。为了阐明这些变化的机制，我们将比较幼稚大鼠和后爪IR损伤大鼠的运动对以下方面的影响：1)通过激光多普勒血流仪和组织氧分压测量后爪肌肉的温度调节和营养血流；2)使用印度墨水灌注法和线粒体氧化能力测量对后爪肌肉毛细血管无复流和肌肉损伤；3)比色法测定后爪肌肉乳酸生成和组织酸中毒；4)非选择性和选择性ASIC拮抗剂对大鼠缺血再灌注损伤的抗伤害作用。

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.