Pape A, Kertscho H, Stein P, Lossen M, Horn O, Kutschker S, Zwissler B, Habler O
Clinic of Anesthesiology, Intensive Care Medicine and Pain Management, J.W. Goethe University Hospital, Frankfurt a.M., Germany.
Eur Surg Res. 2012;48(1):16-25. doi: 10.1159/000333797. Epub 2011 Dec 20.
The patient's individual anemia tolerance is pivotal when blood transfusions become necessary, but are not feasible for some reason. To date, the effects of neuromuscular blockade (NMB) on anemia tolerance have not been investigated.
14 anesthetized and mechanically ventilated pigs were randomly assigned to the Roc group (3.78 mg/kg rocuronium bromide followed by continuous infusion of 1 mg/kg/min, n = 7) or to the Sal group (administration of the corresponding volume of normal saline, n = 7). Subsequently, acute normovolemic anemia was induced by simultaneous exchange of whole blood for a 6% hydroxyethyl starch solution (130/0.4) until a sudden decrease of total body O(2) consumption (VO(2)) indicated a critical limitation of O(2) transport capacity. The Hb concentration quantified at this time point (Hb(crit)) was the primary endpoint of the protocol. Secondary endpoints were parameters of hemodynamics, O(2) transport and tissue oxygenation.
Hb(crit) was significantly lower in the Roc group (2.4 ± 0.5 vs. 3.2 ± 0.7 g/dl) reflecting increased anemia tolerance. NMB with rocuronium bromide reduced skeletal muscular VO(2) and total body O(2) extraction rate. As the cardiac index increased simultaneously, total body VO(2) only decreased marginally in the Roc group (change of VO(2) relative to baseline -1.7 ± 0.8 vs. 3.2 ± 1.9% in the Sal group, p < 0.05).
Deep NMB with rocuronium bromide increases the tolerance of acute normovolemic anemia. The underlying mechanism most likely involves a reduction of skeletal muscular VO(2). During acellular treatment of an acute blood loss, NMB might play an adjuvant role in situations where profound stages of normovolemic anemia have to be tolerated (e.g. bridging an unexpected blood loss until blood products become available for transfusion).
当输血变得必要但由于某些原因不可行时，患者的个体贫血耐受性至关重要。迄今为止，尚未研究神经肌肉阻滞（NMB）对贫血耐受性的影响。
将14只麻醉并机械通气的猪随机分为罗库溴铵组（3.78mg/kg溴化罗库溴铵，随后以1mg/kg/min持续输注，n = 7）或生理盐水组（给予相应体积的生理盐水，n = 7）。随后，通过同时用6%羟乙基淀粉溶液（130/0.4）置换全血诱导急性等容性贫血，直至全身氧耗（VO₂）突然下降表明氧运输能力受到严重限制。此时量化的血红蛋白浓度（Hb(crit)）是该方案的主要终点。次要终点是血流动力学、氧运输和组织氧合参数。
罗库溴铵组的Hb(crit)显著更低（2.4±0.5 vs. 3.2±0.7g/dl），反映出贫血耐受性增加。溴化罗库溴铵进行神经肌肉阻滞降低了骨骼肌VO₂和全身氧摄取率。由于心指数同时增加，罗库溴铵组的全身VO₂仅略有下降（VO₂相对于基线的变化为-1.7±0.8 vs.生理盐水组的3.2±1.9%，p<0.05）。
溴化罗库溴铵深度神经肌肉阻滞可提高急性等容性贫血的耐受性。潜在机制很可能涉及骨骼肌VO₂的降低。在急性失血的无细胞治疗期间，在必须耐受等容性贫血的严重阶段的情况下（例如在意外失血直至有血制品可供输血的过渡期间），神经肌肉阻滞可能起辅助作用。
