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

缺血性损伤导致体感知觉的改变和运动性疼痛的增强。后爪缺血再灌注损伤后，大鼠对机械刺激表现出较低的爪子戒断阈值，这表明运动是痛苦的，运动后大鼠的爪子戒断阈值甚至更低。为了研究这些变化背后的机制，我们将比较运动对naïve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后爪肌肉热调节和营养血流的影响；2)墨汁灌注后爪肌毛细血管无回流和肌肉损伤及线粒体氧化能力测定；3)后爪肌乳酸生成和组织酸中毒用比色法测定及组织pH值；4)非选择性和选择性ASIC拮抗剂对缺血再灌注损伤大鼠的抗伤性作用。

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.