Jänig Wilfrid, Green Paul G
Physiologisches Institut, Christian-Albrechts-Universität zu Kiel, Olshausenstr. 40, D-24098 Kiel, Germany.
University of California, San Francisco, 521 Parnassus Ave, San Francisco, CA 94143-0440, USA.
Auton Neurosci. 2014 May;182:42-54. doi: 10.1016/j.autneu.2014.01.001. Epub 2014 Jan 16.
Inflammation of tissues is under neural control involving neuroendocrine, sympathetic and central nervous systems. Here we used the acute experimental inflammatory model of bradykinin-induced plasma extravasation (BK-induced PE) of the rat knee joint to investigate the neural and neuroendocrine components controlling this inflammation. 1. BK-induced PE is largely dependent on the sympathetic innervation of the synovium, but not on activity in these neurons and not on release of norepinephrine. 2. BK-induced PE is under the control of the hypothalamo-pituitary-adrenal (HPA) system and the sympatho-adrenal (SA) system, activation of both leading to depression of BK-induced PE. The inhibitory effect of the HPA system is mediated by corticosterone and dependent on the sympathetic innervation of the synovium. The inhibitory effect of the SA system is mediated by epinephrine and β2-adrenoceptors. 3. BK-induced PE is inhibited during noxious stimulation of somatic or visceral tissues and is mediated by the neuroendocrine systems. The nociceptive-neuroendocrine reflex circuits are (for the SA system) spinal and spino-bulbo-spinal. 4. The nociceptive-neuroendocrine reflex circuits controlling BK-induced PE are under powerful inhibitory control of vagal afferent neurons innervating the defense line (connected to the gut-associated lymphoid tissue) of the gastrointestinal tract. This inhibitory link between the visceral defense line and the central mechanisms controlling inflammatory mechanisms in body tissues serves to co-ordinate protective defensive mechanisms of the body. 5. The circuits of the nociceptive-neuroendocrine reflexes are under control of the forebrain. In this way, the defensive mechanisms of inflammation in the body are co-ordinated, optimized, terminated as appropriate, and adapted to the behavior of the organism.
组织炎症受神经控制，涉及神经内分泌、交感神经系统和中枢神经系统。在此，我们利用缓激肽诱导大鼠膝关节血浆外渗（BK诱导的PE）的急性实验性炎症模型，来研究控制这种炎症的神经和神经内分泌成分。1. BK诱导的PE在很大程度上依赖于滑膜的交感神经支配，但不依赖于这些神经元的活动，也不依赖于去甲肾上腺素的释放。2. BK诱导的PE受下丘脑-垂体-肾上腺（HPA）系统和交感-肾上腺（SA）系统的控制，两者的激活均导致BK诱导的PE受到抑制。HPA系统的抑制作用由皮质酮介导，并依赖于滑膜的交感神经支配。SA系统的抑制作用由肾上腺素和β2-肾上腺素能受体介导。3. 在对躯体或内脏组织进行伤害性刺激期间，BK诱导的PE受到抑制，且由神经内分泌系统介导。伤害感受性神经内分泌反射回路（对于SA系统而言）是脊髓性的以及脊髓-延髓-脊髓性的。4. 控制BK诱导的PE的伤害感受性神经内分泌反射回路受到支配胃肠道防御线（与肠道相关淋巴组织相连）的迷走传入神经元的强大抑制控制。内脏防御线与控制身体组织炎症机制的中枢机制之间的这种抑制联系有助于协调身体的保护性防御机制。5. 伤害感受性神经内分泌反射回路受前脑控制。通过这种方式，身体炎症的防御机制得以协调、优化、适时终止，并适应机体的行为。
