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虽然痛被用来描述所有真正或潜在的组织损伤或用损伤描述的一种不愉快的感觉和情绪,但实际上痛有两种:第一种是伤害性痛,这种痛是生理性的,与伤害性刺激有关;第二种是临床痛,它有急性与慢性之别。急性痛源于软组织损伤和炎症,具有生物学意义;慢性痛是由神经病理改变所引起的持续性感觉异常,难于治疗。很多分子可能在伤害性痛机制中起重要作用,如经典神经递质、神经肽、质子和三磷酸腺苷等。然而新近的研究结果表明,在周围神经损伤后初级感觉神经细胞中的一氧化氮合酶、神经肽及其受体的表达发生了明显变化,这种初级感觉神经细胞的新的细胞表现型可能与周围神经损伤后常发生慢性痛的起因有关。这些结果有力地提示,慢性痛具有有别于伤害性痛和急性痛的分子和细胞机制。慢性痛研究的快速发展不仅使我们对痛机制有新认识,而且将为治疗慢性痛提供理论基础。
Although pain is used to describe all unpleasant feelings and feelings of all real or potential tissue damage or damage described, there are actually two types of pain: the first is nociceptive pain that is physiological, And nociceptive; second is the clinical pain, it has the difference between acute and chronic. Acute pain from soft tissue injury and inflammation, with biological significance; chronic pain is caused by persistent neuropathological changes in sensory abnormalities, difficult to treat. Many molecules may play an important role in nociceptive pain mechanisms such as classical neurotransmitters, neuropeptides, protons and adenosine triphosphate. However, recent findings suggest that the expression of nitric oxide synthase, neuropeptide and its receptor in primary sensory neurons undergoes significant changes after peripheral nerve injury. The new cell phenotype of this primary sensory nerve cell may And peripheral nerve injury often occurs after the cause of chronic pain. These results strongly suggest that chronic pain has molecular and cellular mechanisms that differ from nociceptive and acute pain. The rapid development of chronic pain research not only gives us new understanding of the pain mechanism, but also provides a theoretical basis for the treatment of chronic pain.