"SCI disrupts the communication between the brainstem vasomotor centres and the regions of the spinal cord that regulate haemodynamics6. The resulting isolation of neurons in the spinal cord triggers a progressive maladaptive reorganization of neuronal projections throughout the spinal cord below the injury that permits the insidious emergence of uncontrolled hypertensive episodes, known as autonomic dysreflexia1. The consequence of these hypertensive episodes is a daily risk of life-threatening cardiovascular events2,3,4,5."
"In humans with SCI, episodes of autonomic dysreflexia are most commonly triggered by bladder or bowel distension, lower urinary tract infections and pressure sores7. We reasoned that identifying the neurons triggering autonomic dysreflexia would require a preclinical model that provokes reliable, repeatable and predictable episodes of autonomic dysreflexia. To establish this model, we elicited autonomic dysreflexia using colorectal distension in mice8 with complete upper-thoracic SCI and monitored pressor responses with beat-by-beat blood pressure monitoring (Fig. 1a,b and Extended Data Fig. 1a-d)."
Spinal cord injury severs communication between brainstem vasomotor centres and spinal regions controlling haemodynamics, leaving isolated spinal neurons that undergo maladaptive reorganization. That reorganization of neuronal projections below the injury enables the emergence of uncontrolled hypertensive episodes termed autonomic dysreflexia, which pose a daily risk of life-threatening cardiovascular events. Common human triggers include bladder or bowel distension, urinary tract infections and pressure sores. A preclinical model used colorectal distension in mice with complete upper-thoracic injury and beat-by-beat blood pressure monitoring to elicit reliable autonomic dysreflexia. Pressor responses emerged around two weeks post-injury and increased to a plateau by one month, persisting at six weeks.
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