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Similar microvascular dysfunction in CRPS patients and animals with chronic post-ischemia pain

机译:在CRPS患者和慢性缺血疼痛后的动物中的类似微血管功能障碍

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There is a growing body of evidence suggesting that CRPS may depend on micro-vascular dysfunction and tissue ischemia secondary to trauma. Skin capillary hemoglobin oxygenation (HbO2) is reduced and skin lactate is increased in CRPS limbs7,17. CRPS patients with cold limbs also have impaired nutritive skin blood flow18. Muscle tissue obtained amputated CRPS limbs were found to exhibit lipofuscin pigment, atrophic fibers, and severely thickened basal membrane layers of the capillaries2,35. Subcutaneous tissue in CRPS limbs exhibit increased density of perfused vessels, lower capillary filtration capacity and arteriovenous shunting21,32. Evidence suggests there is high arterial flow to the CRPS limb, but low oxygen consumption and high lactate flux11. There is also an impairment of high-energy phosphate metabolism and mitochondrial oxygen deficiency in muscle tissue of CRSP limbs14. All of these observations suggest that microvascular dysfunction and ischemia contribute to the induction and maintenance of CRPS.
机译:有一种不断增长的证据表明CRP可能取决于微血管功能障碍和继发于创伤的组织缺血。皮肤毛细血管血红蛋白氧合(HBO2)减少,CRPS肢体7,17中的皮肤乳酸增加。 CRP患有冷肢的患者也受损营养皮肤血液流量18。发现肌肉组织获得截肢的CRPS肢体,表现出唇血素颜料,萎缩纤维和毛细管2,35的严重增厚的基础膜层。 CRPS肢体中的皮下组织表现出增加的灌注血管密度,毛细血管过滤能力和动脉静脉旋转21,32。证据表明CRPS肢体有高动脉流动,但低氧气消耗和高乳酸磁通量11。在CRSP肢体14的肌肉组织中也存在高能磷化代谢和线粒体缺氧的损害。所有这些观察结果表明微血管功能障碍和缺血促进CRP的诱导和维护。

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