高渗盐水溶液在冠状动脉循环中的作用。

Circulatory shock Pub Date : 1994-01-01
G J Crystal, J Gurevicius, S J Kim, P K Eckel, E F Ismail, M R Salem
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引用次数: 0

摘要

未标记:在失血性休克复苏中使用小容量高渗盐水溶液(HSS)可伴随冠脉血流量(CBF)的良好维持和显著增加以及心肌收缩性的增加。本研究在开胸麻醉的狗身上进行,以评估HSS的直接冠状动脉血管扩张剂和正性肌力作用对这些治疗反应的贡献。左冠状动脉前降支(LAD)插管,用正常动脉血恒压(100 mm Hg)灌注。用电磁法测量LAD的脑血流,并计算心肌耗氧量(MVO2)和冠状动脉血浆渗透压。超声晶体法测定LAD床段缩短率(% SS)。在以2 ml/min的速度向LAD中注入2.5、5.0和7.5% HSS时进行测量。这些HSS溶液计算出的血浆渗透压分别为329 +/- 3、361 +/- 8和378 +/- 10 mOsm/kg。2.5% HSS的血浆渗透压升高处于治疗范围,而5.0和7.5% HSS的血浆渗透压升高处于超治疗范围。HSS引起CBF的初始峰值增加(反映冠状动脉血管阻力的降低),在2-3分钟内迅速减弱并达到适度的稳态增加。HSS引起的CBF峰值和稳态增加的幅度与渗透压相关。2.5% HSS对MVO2和% SS没有影响,而5.0%和7.5% HSS以渗透压依赖性的方式增加了这些变量。结论:(1)冠状动脉内输注HSS引起适度的稳态冠状动脉血管舒张;(2)直接的正性肌力效应需要HSS的超治疗性血浆渗透压升高;(3)目前的研究结果表明,HSS的直接心脏作用对使用这些溶液进行失血性休克复苏后冠状动脉血流量和心肌收缩力的增加贡献最小。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of hypertonic saline solutions in the coronary circulation.

Unlabelled: The use of small-volume injections of hypertonic saline solutions (HSS) in resuscitation from hemorrhagic shock is accompanied by well-maintained and pronounced increases in coronary blood flow (CBF) and by increases in myocardial contractility. The present study was performed in open-chest, anesthetized dogs to evaluate the contribution of direct coronary vasodilator and positive inotropic effects of HSS to these therapeutic responses. The left anterior descending coronary artery (LAD) was cannulated and perfused at constant pressure (100 mm Hg) with normal arterial blood. CBF in LAD was measured electromagnetically, and used to calculate myocardial oxygen consumption (MVO2) and coronary arterial plasma osmolality. Percent segmental shortening in LAD bed (% SS) was evaluated with ultrasonic crystals. Measurements were obtained during infusion into LAD of 2.5, 5.0, and 7.5% HSS at 2 ml/min. These HSS solutions yielded calculated plasma osmolalities of 329 +/- 3, 361 +/- 8, and 378 +/- 10 mOsm/kg, respectively. The increases in plasma osmolality by 2.5% HSS were in the therapeutic range, whereas those by 5.0 and 7.5% HSS were supertherapeutic. HSS caused initial peak increases in CBF (reflecting decreases in coronary vascular resistance), which waned rapidly to achieve modest steady-state increases within 2-3 min. The magnitude of the peak and steady-state increases in CBF by HSS correlated to osmolality. The 2.5% HSS had no effect on MVO2 and % SS, whereas the 5.0% and 7.5% HSS increased these variables in an osmolality-dependent manner.

Conclusions: (1) intracoronary infusions of HSS caused modest steady-state coronary vasodilation, (2) Supertherapeutic elevations of plasma osmolality by HSS were required for direct positive inotropic effects, and (3) the present findings suggest that the direct cardiac actions of HSS contribute minimally to the increases in coronary blood flow and myocardial contractility that follow the use of these solutions for resuscitation from hemorrhagic shock.

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