Propofol-induced increase in vascular capacitance is due to inhibition of sympathetic vasoconstrictive activity

Sumio Hoka, Ken Yamaura, Tomoaki Takenaka, Shosuke Takahashi

Research output: Contribution to journalArticle

40 Citations (Scopus)

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 (P(mcf)). The P(mcf) 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 P(mcf) 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 P(mcf) 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 P(mcf) dose-dependently, and (2) the decrease in P(mcf) 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.

Original languageEnglish
Pages (from-to)1495-1500
Number of pages6
JournalAnesthesiology
Volume89
Issue number6
DOIs
Publication statusPublished - Dec 1 1998

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Vascular Capacitance
Propofol
Sympathetic Nervous System
Hypovolemia
Norepinephrine
Arterial Pressure
Controlled Hypotension
Hexamethonium
Urethane
Ketamine
Vasoconstrictor Agents
Heart Atria
Wistar Rats

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

Propofol-induced increase in vascular capacitance is due to inhibition of sympathetic vasoconstrictive activity. / Hoka, Sumio; Yamaura, Ken; Takenaka, Tomoaki; Takahashi, Shosuke.

In: Anesthesiology, Vol. 89, No. 6, 01.12.1998, p. 1495-1500.

Research output: Contribution to journalArticle

Hoka, Sumio ; Yamaura, Ken ; Takenaka, Tomoaki ; Takahashi, Shosuke. / Propofol-induced increase in vascular capacitance is due to inhibition of sympathetic vasoconstrictive activity. In: Anesthesiology. 1998 ; Vol. 89, No. 6. pp. 1495-1500.
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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 (P(mcf)). The P(mcf) 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 P(mcf) 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 P(mcf) 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 P(mcf) dose-dependently, and (2) the decrease in P(mcf) 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.",
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