title: Acute changes in systemic hemodynamics and serum vasopressin after complete cervical spinal cord injury in piglets.
abstract: BACKGROUND
  Spinal cord injury (SCI) produces acute hemodynamic alterations through disruption of sympathetic output of the autonomic nervous system and places individuals with SCI at high risk of secondary ischemic insult to the spinal cord as well as to other organs. The purpose of this study was to examine hemodynamics and serum vasopressin concentration in the acute period following complete cervical SCI in piglets.
  
  
  METHODS
  We developed a new model of traumatic complete cervical SCI in piglets and measured acute hemodynamic variables and serum arginine vasopressin (AVP) concentrations at baseline and for 4 h after SCI under fentanyl anesthesia.
  
  
  RESULTS
  Complete cervical SCI caused an immediate tachycardia which lasted for approximately 1 h, immediate hypotension which was sustained for the 4-h duration of the study, decreases in both systemic and pulmonary vascular resistance, and a compensatory increase in cardiac output, which resulted initially from an increase in heart rate (HR) but was later sustained after resolution of tachycardia by an increase in cardiac stroke volume. Serum AVP concentration increased significantly after SCI and did not change in the control group. Neurogenic shock did not occur due to the robust increase in cardiac output and cardiac stroke volume.
  
  
  CONCLUSIONS
  Complete cervical SCI produces hemodynamic alterations consistent with the withdrawal of sympathetic tone. Although mean arterial pressure (MAP) decreased significantly after SCI, the increase in serum vasopressin may have played a role in maintaining blood pressure and preventing circulatory collapse, a complication which is encountered frequently in patients with cervical and upper thoracic SCI.
authors.affiliation: Saint Louis University School of Medicine, Saint Louis, MO, USA.
authors.forename: Michael
authors.initials: M
authors.lastname: Zahra
authors.forename: Amer
authors.initials: A
authors.lastname: Samdani
authors.forename: Kurt
authors.initials: K
authors.lastname: Piggott
authors.forename: Manuel
authors.initials: M
authors.lastname: Gonzalez-Brito
authors.forename: Juan
authors.initials: J
authors.lastname: Solano
authors.forename: Roosevelt
authors.initials: R
authors.lastname: De Los Santo
authors.forename: Juan C
authors.initials: JC
authors.lastname: Buitrago
authors.forename: Farid
authors.initials: F
authors.lastname: Alam
authors.forename: Dansha
authors.initials: D
authors.lastname: He
authors.forename: John P
authors.initials: JP
authors.lastname: Gaughan
authors.forename: Randal
authors.initials: R
authors.lastname: Betz
authors.forename: Dalton
authors.initials: D
authors.lastname: Dietrich
authors.forename: John
authors.initials: J
authors.lastname: Kuluz
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001127:Arginine Vasopressin / Q000097:blood*; D001794:Blood Pressure; D002302:Cardiac Output; D002574:Cervical Vertebrae; D006339:Heart Rate; D006439:Hemodynamics; D008279:Magnetic Resonance Imaging; D011652:Pulmonary Circulation; D013116:Spinal Cord / Q000473:pathology; D013119:Spinal Cord Injuries / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology*; D013318:Stroke Volume; D013552:Swine; D013997:Time Factors; D014655:Vascular Resistance
chemical_list: D001127:Arginine Vasopressin
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