title: Propofol-induced increase in vascular capacitance is due to inhibition of sympathetic vasoconstrictive activity.
abstract: BACKGROUND
  Venodilation is thought to be one of the mechanisms underlying propofol-induced hypotension. The purpose of this study is to test two hypotheses: (1) propofol increases systemic vascular capacitance, and (2) the capacitance change produced by propofol is a result of an inhibition of sympathetic vasoconstrictor activity.
  
  
  METHODS
  In 33 Wistar rats previously anesthetized with urethane and ketamine, vascular capacitance was examined before and after propofol infusion by measuring mean circulatory filling pressure (Pmcf). The Pmcf was measured during a brief period of circulatory arrest produced by inflating an indwelling balloon in the right atrium. Rats were assigned into four groups: an intact group, a sympathetic nervous system (SNS)-block group produced by hexamethonium infusion, a SNS-block + noradrenaline (NA) group, and a hypovolemic group. The Pmcf was measured at a control state and 2 min after a bolus administration of 2, 10, and 20 mg/kg of propofol.
  
  
  RESULTS
  The mean arterial pressure (MAP) was decreased by propofol dose-dependently in intact, hypovolemic, and SNS-block groups, but the decrease in MAP was less in the SNS-block group (-25%) than in the intact (-50%) and hypovolemic (-61%) groups. In the SNS-block + NA group, MAP decreased only at 20 mg/kg of propofol (-18%). The Pmcf decreased in intact and hypovolemic groups in a dose-dependent fashion but was unchanged in the SNS-block and SNS-block + NA groups.
  
  
  CONCLUSIONS
  The results have provided two principal findings: (1) propofol decreases Pmcf dose-dependently, and (2) the decrease in Pmcf by propofol is elicited only when the sympathetic nervous system is intact, suggesting that propofol increases systemic vascular capacitance as a result of an inhibition of sympathetic nervous system.
authors.affiliation: Department of Anesthesiology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan. shoka@med.kitasato-u.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Hoka
authors.forename: K
authors.initials: K
authors.lastname: Yamaura
authors.forename: T
authors.initials: T
authors.lastname: Takenaka
authors.forename: S
authors.initials: S
authors.lastname: Takahashi
mesh_terms: D018686:Anesthetics, Intravenous / Q000494:pharmacology*; D000818:Animals; D001340:Autonomic Nerve Block; D001794:Blood Pressure / Q000187:drug effects; D003864:Depression, Chemical; D004305:Dose-Response Relationship, Drug; D006339:Heart Rate / Q000187:drug effects; D005996:Nitroglycerin / Q000494:pharmacology; D015742:Propofol / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013564:Sympathetic Nervous System / Q000187:drug effects*; D018924:Vascular Capacitance / Q000187:drug effects*; D014661:Vasoconstriction / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D018686:Anesthetics, Intravenous; D014665:Vasodilator Agents; D005996:Nitroglycerin; D015742:Propofol