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

作者: Sumio Hoka , Ken Yamaura , Tomoaki Takenaka , Shosuke Takahashi

DOI: 10.1097/00000542-199812000-00028

关键词: Vascular CapacitanceKetamineMean circulatory filling pressureMean arterial pressureHemodynamicsPropofolInternal medicineMedicineSympathetic nervous systemEndocrinologyHexamethonium

摘要: Background: Venodilation is thought to be one of the mechanisms underlying propofol-induced hypotension. The purpose this study test two hypotheses: (1) propofol increases systemic vascular capacitance, and (2) capacitance change produced by a result an inhibition sympathetic vasoconstrictor activity. Methods: In 33 Wistar rats previously anesthetized with urethane ketamine, was examined before after infusion measuring mean circulatory filling pressure (P mcf ). P measured during brief period arrest inflating indwelling balloon in right atrium. Rats were assigned into four groups: intact group, nervous system (SNS)-block group hexamethonium infusion, SNS-block + noradrenaline (NA) hypovolemic group. at control state 2 min bolus administration 2, 10, 20 mg/kg propofol. Results: arterial (MAP) decreased dose-dependently intact, hypovolemic, groups, but decrease MAP less (-25%) than (-50%) (-61%) groups. NA only (-18%). groups dose-dependent fashion unchanged Conclusions: results have provided principal findings : decreases dose-dependently, elicited when suggesting that as system.

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