title: Pathology influences blood pressure change following vagal stimulation in an animal intubation model.
abstract: OBJECTIVE
  The haemodynamic response to critical care intubation is influenced by the use of sedation and relaxant drugs and the activation of the vagal reflex. It has been hypothesized that different disease states may have a contrasting effect on the cardiovascular response to vagal stimulation. Our objective was to determine whether the blood pressure response to vagal stimulation was modified by endotoxaemia or hypovolaemia.
  
  
  METHODS
  New Zealand White rabbits were anaesthetised with urethane before tracheotomy. The exposed left Vagus nerve of randomised groups of control (n = 11), endotoxin (n = 11, 1 mg/kg), hypovolaemia 40% (n = 8) and hypovolaemia 20% (n = 8) rabbits were subjected to 10 Hz pulsed electrical stimulations of 25 s duration every 15 min. Haemodynamic parameters were recorded from a catheter in the right carotid artery connected to an iWorx monitor. Serum catecholamines were measured every 30 min using reverse-phase ion-pairing liquid chromatography. The change in blood pressure after vagal stimulation was compared to controls for one hour after the first death in the experimental groups.
  
  
  RESULTS
  29% of the rabbits died in the hypovolaemia 40% group and 27% in the endotoxin group. One rabbit died in the hypovolaemia 40% group before vagal stimulation and was excluded. Following electrical stimulation of the Vagus nerve there was a fall in blood pressure in control rabbits. Blood pressure was conserved in the hypovolaemic rabbits compared to controls (p<0.01). For the endotoxaemic rabbits, there was a non-significant trend for the mean blood pressure to decrease more than the controls. Serum catecholamines were significantly raised in both the hypovolaemic and endotoxaemic rabbits.
  
  
  CONCLUSIONS
  Pathology may contribute to modifications in blood pressure when vagal activation occurs. Patients who are either already vasoconstricted, or not vasoplegic, may be less at risk from intubation-related vagally mediated reductions in blood pressure than those with vasodilatory pathologies.
authors.affiliation: Critical Care Group - Portex Unit, Institute of Child Health, University College London, United Kingdom ; Assistance Publique-Hôpitaux de Paris, Réanimation Pédiatrique, Hôpital Robert Debré, Paris, France.
authors.forename: Peter
authors.initials: P
authors.lastname: Jones
authors.forename: Laurent
authors.initials: L
authors.lastname: Guillaud
authors.forename: Christophe
authors.initials: C
authors.lastname: Desbois
authors.forename: Jean-Francois
authors.initials: JF
authors.lastname: Benoist
authors.forename: Helene
authors.initials: H
authors.lastname: Combrisson
authors.forename: Stephane
authors.initials: S
authors.lastname: Dauger
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Peters
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002318:Cardiovascular Diseases; D002319:Cardiovascular System; D002339:Carotid Arteries / Q000473:pathology; D002395:Catecholamines / Q000378:metabolism; D002853:Chromatography, Liquid; D019446:Endotoxemia / Q000378:metabolism; D006339:Heart Rate; D006400:Hematocrit; D006439:Hemodynamics; D020896:Hypovolemia; D007442:Intubation, Intratracheal; D008297:Male; D023421:Models, Animal; D011817:Rabbits; D014630:Vagus Nerve / Q000378:metabolism / Q000502:physiology*; D014661:Vasoconstriction
chemical_list: D002395:Catecholamines