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异丙酚对犬左心室-动脉耦合及机械效率的影响。

Alterations in canine left ventricular-arterial coupling and mechanical efficiency produced by propofol.

作者信息

Hettrick D A, Pagel P S, Warltier D C

机构信息

Medical College of Wisconsin, Milwaukee 53226, USA.

出版信息

Anesthesiology. 1997 May;86(5):1088-93. doi: 10.1097/00000542-199705000-00012.

DOI:10.1097/00000542-199705000-00012
PMID:9158358
Abstract

BACKGROUND

Propofol reduces blood pressure by decreasing left ventricular (LV) afterload and myocardial contractility. This investigation tested the hypothesis that propofol preserves LV-arterial coupling and mechanical efficiency because of these simultaneous hemodynamic actions.

METHODS

Experiments were conducted in open-chest dogs (n = 8) instrumented for measurement of aortic and LV pressure, dP/dtmax, and LV volume. Myocardial contractility was assessed with the slope (Ees) of the LV end systolic pressure-volume relationship. Effective arterial elastance (En; the ratio of end systolic arterial pressure to stroke volume), stroke work (SW), and pressure-volume area (PVA) were determined from the LV pressure-volume relationships. Dogs were studied 30 min after instrumentation and after 15-min intravenous infusions of propofol at 5, 10, 20, and 40 mg.kg-1.h-1.

RESULTS

Propofol caused dose-dependent decreases in Ees (4.7 +/- 0.9 during control to 2.7 +/- 0.5 mmHg/ml during the high dosage) and dP/dtmax, indicating a direct negative inotropic effect. Ea increased at the 10 mg.kg-1.h-1 dose of propofol but decreased at higher dosages. Propofol decreased the ratio of Ees to Ea (0.88 +/- 0.13 during control to 0.56 +/- 0.10 during the high dosage), consistent with impairment of LV-arterial coupling. Propofol also reduced the ratio SW to PVA (0.54 +/- 0.03 during control to 0.45 +/- 0.03 during the 20 mg.kg-1.h-1), suggesting a decline in LV mechanical efficiency. SW and PVA recovered toward baseline values at the 40 mg.kg-1.h-1 dose.

CONCLUSIONS

Although propofol depresses mechanical matching of the LV to the arterial system and reduces LV efficiency, these alterations plateau at higher dosages of propofol because reductions in afterload begin to offset further declines in myocardial contractile function.

摘要

背景

丙泊酚通过降低左心室(LV)后负荷和心肌收缩力来降低血压。本研究检验了这样一个假设,即由于这些同时发生的血流动力学作用,丙泊酚可维持左心室 - 动脉耦合及机械效率。

方法

在开胸犬(n = 8)身上进行实验,这些犬安装了用于测量主动脉和左心室压力、dP/dtmax以及左心室容积的仪器。通过左心室收缩末期压力 - 容积关系的斜率(Ees)评估心肌收缩力。根据左心室压力 - 容积关系确定有效动脉弹性(En;收缩末期动脉压与每搏量之比)、每搏功(SW)和压力 - 容积面积(PVA)。在安装仪器30分钟后以及以5、10、20和40mg·kg-1·h-1的剂量静脉输注丙泊酚15分钟后对犬进行研究。

结果

丙泊酚导致Ees(对照期间为4.7±0.9,高剂量期间为2.7±0.5mmHg/ml)和dP/dtmax呈剂量依赖性降低,表明直接的负性肌力作用。在丙泊酚剂量为10mg·kg-1·h-1时Ea升高,但在更高剂量时降低。丙泊酚降低了Ees与Ea的比值(对照期间为

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