DOI: 10.1016/S0079-6123(05)52017-X
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摘要: Spinal cord injuries above mid-thoracic levels can lead to a potentially life-threatening hypertensive condition termed autonomic dysreflexia that is often triggered by distension of pelvic viscera (bladder or bowel). This syndrome characterized episodic hypertension due sudden, massive discharge sympathetic preganglionic neurons in the thoracolumbar spinal cord. usually accompanied bradycardia, particularly if injury caudal 2nd 4th thoracic segments. The development correlated with aberrant sprouting peptidergic afferent fibers into below injury. In particular, nerve growth factor-responsive has been shown have major influence on dysreflexia, perhaps amplifying activation disinhibited neurons. Using model noxious bowel after complete transection at segment rats, we selectively altered C-fiber sprouting, specified injury, microinjections adenovirus encoding growth-promoting factor growth-inhibitory semaphorin 3A. was followed assessment physiological responses colorectal and subsequent histology. Additionally, anterograde tract tracers were injected lumbosacral region compare extent labeled propriospinal rostral projections uninjured cords those transection. summary, overexpression chemorepulsive 3A impeded segments mitigated whereas opposite results obtained overexpression. Furthermore, compared naive there significantly more rostrally Collectively, our findings suggest increases excitation expanded terminals This, turn, triggers local relay visceral sensory stimuli amplify cord, enhance transmission viscero-sympathetic reflex pathway. These are manifested as dysreflexia.