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首页> 外文期刊>Resuscitation. >Effects of levosimendan in normodynamic endotoxaemia: a controlled experimental study.
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Effects of levosimendan in normodynamic endotoxaemia: a controlled experimental study.

机译：左西孟旦在正常动力内毒素血症中的作用：一项对照实验研究。

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OBJECTIVES: Levosimendan is an inotropic and vasodilator drug that has proved to be useful in cardiogenic shock. Pretreatment with levosimendan in experimental hypodynamic septic shock in pigs has shown valuable effects in oxygen transport. Our goal was to assess the effects of levosimendan in a normodynamic model of endotoxaemia. METHODS: Twelve sheep were anaesthetized and mechanically ventilated. After taking basal haemodynamic and oxygen transport measurements, sheep were assigned to two groups during 120 min: (1) endotoxin (5 microg/kg endotoxin); (2) levosimendan (5 microg/kg endotoxin plus levosimendan 200 microg/kg followed by 200 microg/kg/h). Both groups received hydration of 20 ml/kg/h of saline solution. RESULTS: In the endotoxin group, cardiac output, intestinal blood flow and systemic and intestinal oxygen transports and consumptions (DO(2) and VO(2)) remained unchanged. In the levosimendan group, systemic and intestinal DO(2) were significantly higher than in the endotoxin group. Because stroke volume did not change (basal versus 120': 0.9+/-0.1 ml/kg versus 0.9+/-0.2 ml/kg, p=0.3749), the elevation in cardiac output by levosimendan (145+/-17 ml/min/kg versus 198+/-16 ml/min/kg, p=0.0096) was related to an increased heart rate (159+/-32 beats l/min versus 216+/-19 beats l/min, p=0.0037). Levosimendan precluded the development of gut intramucosal acidosis at 120' (endotoxin versus levosimendan, ileal intramucosal-arterial [Formula: see text] difference: 19+/-4 Torr versus 10+/-4 Torr, p=0.0025). However, levosimendan decreased mean arterial blood pressure (99+/-20 Torr versus 63+/-13 Torr, p=0.0235) and increased blood lactate levels (2.4+/-0.9 mmol/l versus 4.8+/-1.5 mmol/l, p=0.0479). All p-values are differences in specific points (paired or unpaired t-test with Bonferroni correction) after two-way repeated measures ANOVA. A p-value<0.05 was considered significant. CONCLUSIONS: Levosimendan improved oxygen transport and prevented the development of intramucosal acidosis in this experimental model of endotoxaemia. However, systemic hypotension and lactic acidosis occurred. Additional studies are needed to show if different doses and timing of levosimendan administration in septic shock might improve gut perfusion without adverse effects.
机译：目的：左西孟旦是一种正性肌力药物和血管扩张药，已被证明可用于心源性休克。左西孟旦对猪实验性低动力性败血性休克的预处理已显示出对氧气转运的重要作用。我们的目标是评估左西孟旦在内毒素血症正常动力学模型中的作用。方法：对十二只绵羊进行麻醉和机械通气。在进行基础血流动力学和氧气输送测量后，在120分钟内将绵羊分为两组：（1）内毒素（5 microg / kg内毒素）; （2）左西孟旦（5微克/千克内毒素加左西孟旦200微克/千克，然后是200微克/千克/小时）。两组均接受20 ml / kg / h盐溶液的水合作用。结果：内毒素组中，心输出量，肠血流量以及全身和肠中的氧气运输和消耗（DO（2）和VO（2））保持不变。在左西孟旦组，全身和肠道的DO（2）明显高于内毒素组。因为中风量没有变化（基础值相对于120'：0.9 +/- 0.1 ml / kg对0.9 +/- 0.2 ml / kg，p = 0.3749），所以左西孟旦会增加心输出量（145 +/- 17 ml / kg min / kg对198 +/- 16 ml / min / kg，p = 0.0096）与心律增加有关（159 +/- 32次l / min对216 +/- 19次l / min，p = 0.0037 ）。左西孟旦排除了肠道在120'时粘膜内酸中毒的发展（内毒素与左西孟旦，回肠粘膜内动脉[配方：见正文]差异：19 +/- 4 Torr对10 +/- 4 Torr，p = 0.0025）。然而，左西孟旦降低了平均动脉血压（99 +/- 20 Torr对63 +/- 13 Torr，p = 0.0235）并提高了血液乳酸水平（2.4 +/- 0.9 mmol / l对4.8 +/- 1.5 mmol / l） ，p = 0.0479）。所有p值都是经过两次重复测量方差分析后特定点的差异（配对或不配对的t检验，采用Bonferroni校正）。 P值<0.05被认为是显着的。结论：左西孟旦改善了该内毒素血症实验模型中的氧运输并防止了粘膜内酸中毒的发展。但是，发生全身性低血压和乳酸性酸中毒。还需要进一步的研究，以证明在败血性休克中不同剂量和时间的左西孟旦给药可以改善肠道灌注而无不良影响。

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