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麻醉诱导对心肌功能和代谢的影响:芬太尼、舒芬太尼和阿芬太尼的比较

Effects of anesthetic induction on myocardial function and metabolism: a comparison of fentanyl, sufentanil and alfentanil.

作者信息

Miller D R, Wellwood M, Teasdale S J, Laidley D, Ivanov J, Young P, Madonik M, McLaughlin P, Mickle D A, Weisel R D

机构信息

Division of Clinical Biochemistry, Toronto General Hospital, University of Toronto, Ontario.

出版信息

Can J Anaesth. 1988 May;35(3 ( Pt 1)):219-33. doi: 10.1007/BF03010615.

Abstract

Anaesthetic induction may induce myocardial ischaemia. A prospective randomized trial was instituted to compare the effect on ventricular function and myocardial metabolism of induction with fentanyl (FEN) or its analogues sufentanil (SUF) or alfentanil (ALF) in 96 patients undergoing elective coronary artery bypass grafting (CABG). Haemodynamic, metabolic (coronary sinus oxygen and lactate extraction) and gated ventriculographic measurements were made awake pre-induction (PRE), after induction (IND) and after intubation (INT). Induction was performed with FEN 75 micrograms.kg-1, SUF 15 micrograms.kg-1 or ALF 125 micrograms.kg-1 and metocurine. Fentanyl induction was associated with the greatest stability of mean arterial pressure (MAP), cardiac performance, and systolic function without associated myocardial lactate production. SUF produced the greatest depression of systolic function (p less than 0.05) but without haemodynamic instability or myocardial lactate production in all but one patient. Induction with ALF produced the greatest reduction in MAP (p less than 0.05) associated with the greatest decrease in diastolic compliance (p less than 0.05) and 50 per cent incidence of myocardial lactate production (p less than 0.05) with no significant change in coronary blood flow or myocardial oxygen consumption.

摘要

麻醉诱导可能会诱发心肌缺血。开展了一项前瞻性随机试验,以比较芬太尼(FEN)及其类似物舒芬太尼(SUF)或阿芬太尼(ALF)对96例行择期冠状动脉旁路移植术(CABG)患者的心室功能和心肌代谢的诱导效果。在诱导前清醒状态(PRE)、诱导后(IND)和插管后(INT)进行血流动力学、代谢指标(冠状窦氧和乳酸摄取)和门控心室造影测量。诱导采用75微克·千克-1的芬太尼、15微克·千克-1的舒芬太尼或125微克·千克-1的阿芬太尼及美托库铵。芬太尼诱导与平均动脉压(MAP)、心脏功能和收缩功能的最大稳定性相关,且无相关心肌乳酸生成。舒芬太尼导致收缩功能的最大程度抑制(p<0.05),但除1例患者外,所有患者均无血流动力学不稳定或心肌乳酸生成。阿芬太尼诱导导致MAP的最大降幅(p<0.05),同时伴有舒张顺应性的最大降幅(p<0.05)和50%的心肌乳酸生成发生率(p<0.05),而冠状动脉血流或心肌氧耗无显著变化。

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