Hernández Glenn, Tapia Pablo, Alegría Leyla, Soto Dagoberto, Luengo Cecilia, Gomez Jussara, Jarufe Nicolas, Achurra Pablo, Rebolledo Rolando, Bruhn Alejandro, Castro Ricardo, Kattan Eduardo, Ospina-Tascón Gustavo, Bakker Jan
Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, 8320000, Chile.
Unidad de Pacientes Críticos, Hospital Clínico Universidad de Chile Santos Dumont 999, Santiago, 8380000, Chile.
Crit Care. 2016 Aug 2;20(1):234. doi: 10.1186/s13054-016-1419-x.
Persistent hyperlactatemia during septic shock is multifactorial. Hypoperfusion-related anaerobic production and adrenergic-driven aerobic generation together with impaired lactate clearance have been implicated. An excessive adrenergic response could contribute to persistent hyperlactatemia and adrenergic modulation might be beneficial. We assessed the effects of dexmedetomidine and esmolol on hemodynamics, lactate generation, and exogenous lactate clearance during endotoxin-induced septic shock.
Eighteen anesthetized and mechanically ventilated sheep were subjected to a multimodal hemodynamic/perfusion assessment including hepatic and portal vein catheterizations, total hepatic blood flow, and muscle microdialysis. After monitoring, all received a bolus and continuous infusion of endotoxin. After 1 h they were volume resuscitated, and then randomized to endotoxin-control, endotoxin-dexmedetomidine (sequential doses of 0.5 and 1.0 μg/k/h) or endotoxin-esmolol (titrated to decrease basal heart rate by 20 %) groups. Samples were taken at four time points, and exogenous lactate clearance using an intravenous administration of sodium L-lactate (1 mmol/kg) was performed at the end of the experiments.
Dexmedetomidine and esmolol were hemodynamically well tolerated. The dexmedetomidine group exhibited lower epinephrine levels, but no difference in muscle lactate. Despite progressive hypotension in all groups, both dexmedetomidine and esmolol were associated with lower arterial and portal vein lactate levels. Exogenous lactate clearance was significantly higher in the dexmedetomidine and esmolol groups.
Dexmedetomidine and esmolol were associated with lower arterial and portal lactate levels, and less impairment of exogenous lactate clearance in a model of septic shock. The use of dexmedetomidine and esmolol appears to be associated with beneficial effects on gut lactate generation and lactate clearance and exhibits no negative impact on systemic hemodynamics.
脓毒性休克期间持续高乳酸血症是多因素导致的。与低灌注相关的无氧产生、肾上腺素能驱动的有氧生成以及乳酸清除受损都与之相关。过度的肾上腺素能反应可能导致持续高乳酸血症，而肾上腺素能调节可能有益。我们评估了右美托咪定和艾司洛尔在内毒素诱导的脓毒性休克期间对血流动力学、乳酸生成和外源性乳酸清除的影响。
18只麻醉并机械通气的绵羊接受了多模式血流动力学/灌注评估，包括肝静脉和门静脉插管、肝总血流量以及肌肉微透析。监测后，所有绵羊均接受内毒素推注和持续输注。1小时后进行容量复苏，然后随机分为内毒素对照组、内毒素 - 右美托咪定组（依次给予0.5和1.0μg / kg / h剂量）或内毒素 - 艾司洛尔组（滴定至基础心率降低20%）。在四个时间点采集样本，并在实验结束时通过静脉注射L - 乳酸钠（1 mmol / kg）进行外源性乳酸清除。
右美托咪定和艾司洛尔在血流动力学方面耐受性良好。右美托咪定组肾上腺素水平较低，但肌肉乳酸无差异。尽管所有组均出现进行性低血压，但右美托咪定和艾司洛尔均与较低的动脉和门静脉乳酸水平相关。右美托咪定组和艾司洛尔组的外源性乳酸清除率显著更高。
在脓毒性休克模型中，右美托咪定和艾司洛尔与较低的动脉和门静脉乳酸水平相关，且对外源性乳酸清除的损害较小。右美托咪定和艾司洛尔的使用似乎对肠道乳酸生成和乳酸清除有有益影响，且对全身血流动力学无负面影响。
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