title: Recurrent autonomic dysreflexia exacerbates vascular dysfunction after spinal cord injury.
abstract: BACKGROUND
  Individuals with high spinal cord injury (SCI) are prone to significant fluctuation in blood pressure with episodes of very high and low blood pressure during autonomic dysreflexia (AD) and orthostatic hypotension, respectively. We do not know how such blood pressure lability affects the vasculature.
  
  
  OBJECTIVE
  We used a well-characterized animal model of AD to determine whether increasing the frequency of AD during recovery from SCI would exacerbate injury-induced dysfunction in resistance vessels.
  
  
  METHODS
  Experimental animal study. International Collaboration On Repair Discoveries (ICORD), University of British Columbia, Canada.
  
  
  METHODS
  Complete transection of the T3 spinal cord was performed in male Wistar rats. For 14 days after injury, AD was induced via colorectal distension (CRD; 30 minutes per day) in the experimental group (SCI-CRD). One month after SCI, baseline cardiovascular parameters and severity of CRD-induced AD were assessed in SCI-CRD animals and SCI-only controls. Mesenteric arteries were harvested for in vitro myography to characterize vasoactive responses to phenylephrine (PE) and acetylcholine (ACh).
  
  
  RESULTS
  Mesenteric arteries from SCI-CRD animals exhibited larger maximal responses to PE than arteries from SCI-only controls. Hyperresponsiveness to PE was not a product of endothelial dysfunction because mesenteric arteries from both groups had similar vasodilator responses to ACh. Both SCI-only controls and SCI-CRD animals exhibited CRD-evoked AD 1 month after SCI; however, CRD-induced hypertension was less pronounced in animals that were previously exposed to CRD.
  
  
  CONCLUSIONS
  Injury-induced changes within the vasculature may contribute to the development of AD after SCI. Here, we provide evidence that AD itself has significant and long-lasting effects on vascular function. This finding has implications for the medical management of AD and provides an impetus for maintaining stable blood pressure.
authors.affiliation: International Collaboration on Repair Discoveries (ICORD), University of British Columbia, Blusson Spinal Cord Centre, Vancouver, British Columbia, Canada.
authors.forename: Nima
authors.initials: N
authors.lastname: Alan
authors.forename: Leanne M
authors.initials: LM
authors.lastname: Ramer
authors.forename: Jessica A
authors.initials: JA
authors.lastname: Inskip
authors.forename: Saeid
authors.initials: S
authors.lastname: Golbidi
authors.forename: Matt S
authors.initials: MS
authors.lastname: Ramer
authors.forename: Ismail
authors.initials: I
authors.lastname: Laher
authors.forename: Andrei V
authors.initials: AV
authors.lastname: Krassioukov
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D020211:Autonomic Dysreflexia / Q000150:complications* / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008297:Male; D009213:Myography; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000150:complications* / Q000503:physiopathology; D013904:Thoracic Vertebrae; D014652:Vascular Diseases / Q000209:etiology* / Q000503:physiopathology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D000109:Acetylcholine