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首页> 外文期刊>Progress in brain research >Adaptations of peripheral vasoconstrictor pathways after spinal cord injury.
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Adaptations of peripheral vasoconstrictor pathways after spinal cord injury.

机译：脊髓损伤后外周血管收缩途径的适应性。

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The consequences of spinal cord injury on the function of sympathetic pathways in the periphery have generally been ignored. We discuss two types of plasticity that follow disruption of sympathetic pathways in rats . The first relates to the partial denervation of sympathetic ganglia that would follow the loss of some preganglionic neurones. Sprouting of residual connections rapidly reinnervates many postganglionic neurones, restoring functional transmission within a few weeks, but other neurones may be permanently decentralized. Some of the new functional connections may generate inappropriate pathways leading to abnormal reflexes . The second type of plasticity concerns the markedly enhanced and prolonged contractile responses to nerve activity in arterial vessels to which ongoing sympathetic activity has been reduced or silenced following spinal cord transection or ganglion decentralization. In a cutaneous artery (the rat tail artery), the mechanisms underlying this arterial hyperreactivity differ from those in the splanchnic arteries (the rat mesenteric artery). In the former, hyperreactivity is mainly postjunctional but independent of changes in alpha1-adrenoceptor sensitivity, whereas the increased responsiveness in the latter vessels can be attributed to a greater responsiveness to alpha1-adrenoceptor activation. There are enough data from humans to suggest that both of these novel findings in experimental animals are likely to apply after spinal cord injury and contribute to autonomic dysreflexia .
机译：脊髓损伤对周围交感途径功能的影响通常被忽略。我们讨论了遵循大鼠交感途径破坏的两种可塑性。第一个问题涉及交感神经节的部分神经支配，继发于某些神经节前神经元的丧失。残留连接的发芽迅速使许多神经节后神经元重新受神经支配，在数周内恢复了功能传递，但其他神经元可能会永久分散。一些新的功能连接可能会产生不适当的途径，导致异常反射。第二种可塑性涉及在脊髓横切或神经节分散之后，对动脉血管中神经活动的明显增强和延长的收缩反应，而对这些活动的持续交感神经活动已被减少或沉默。在皮肤动脉（大鼠尾动脉）中，这种动脉过度反应的机制与内脏动脉（大鼠肠系膜动脉）的机制不同。在前者中，反应过度主要是结后的，但不依赖于α1-肾上腺素受体敏感性的变化，而后者的血管反应性增强可归因于对α1-肾上腺素受体激活的更大反应性。来自人类的足够的数据表明，实验动物的这些新发现都可能在脊髓损伤后应用，并导致自主神经反射不良。

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