title: Recovery of baroreflex control of renal sympathetic nerve activity after spinal lesions in the rat.
abstract: Spinal cord injury (SCI) has serious long-term consequences on sympathetic cardiovascular regulation. Orthostatic intolerance results from insufficient baroreflex regulation (BR) of sympathetic outflow to maintain proper blood pressure upon postural changes. Autonomic dysreflexia occurs due to insufficient inhibition of spinal sources of sympathetic activity. Both of these conditions result from the inability to control sympathetic activity caudal to SCI. It is well established that limited motor ability recovers after incomplete SCI. Therefore, the goal of this study was to determine whether recovery of BR occurs after chronic, left thoracic spinal cord hemisection at either T(3) or T(8). Baroreflex tests were performed in rats by measuring the reflex response of left (ipsilateral) renal sympathetic nerve activity to decreases and increases in arterial pressure produced by ramped infusions of sodium nitroprusside and phenylephrine, respectively. One week after a T(3) left hemisection, BR function was modestly impaired. However, 8 wk after a T(3) left hemisection, BR function was normal. One week after a T(8) left hemisection, BR function was significantly impaired, and 8 wk after a T(8) left hemisection, BR function was significantly improved. These results indicate that BR of renal sympathetic nerve activity in rats may partially recover after spinal cord hemisections, becoming normal by 8 wk after a T(3) lesion, but not after a T(8) lesion. The nature of the spinal cord and/or brain stem reorganization that mediates this recovery remains to be determined.
authors: Dept. of Biomedical Engineering, The Johns Hopkins Univ. School of Medicine, 605 Traylor Bldg., 720 Rutland Ave., Baltimore, MD 21205, USA. mzahner1@jhmi.edu
authors: Matthew R
authors: MR
authors: Zahner
authors: Ewa
authors: E
authors: Kulikowicz
authors: Lawrence P
authors: LP
authors: Schramm
mesh_terms: D000818:Animals; D020211:Autonomic Dysreflexia / Q000209:etiology / Q000503:physiopathology*; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D007262:Infusions, Intravenous; D007668:Kidney / Q000294:innervation*; D009599:Nitroprusside / Q000008:administration & dosage; D054971:Orthostatic Intolerance / Q000209:etiology / Q000503:physiopathology*; D010656:Phenylephrine / Q000008:administration & dosage; D011187:Posture; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D013119:Spinal Cord Injuries / Q000209:etiology / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology*; D013904:Thoracic Vertebrae / Q000601:surgery; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000008:administration & dosage; D014665:Vasodilator Agents / Q000008:administration & dosage
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine