Luyer Misha D P, Jacobs Jan A, Vreugdenhil Anita C E, Hadfoune M'hamed, Dejong Cornelis H C, Buurman Wim A, Greve Jan Willem M
Department of Surgery, University of Maastricht and University Hospital Maastricht, the Netherlands.
Ann Surg. 2004 Feb;239(2):257-64. doi: 10.1097/01.sla.0000108695.60059.80.
To determine whether potential enhancement of endotoxin neutralization via high-fat enteral nutrition affects endotoxemia and bacterial translocation after hemorrhage.
Endotoxin and bacterial translocation due to gut barrier failure are important initiating events in the pathogenesis of sepsis after hemorrhage. Systemic inhibition of endotoxin activity attenuates bacterial translocation and distant organ damage. Triacylglycerol-rich lipoproteins constitute a physiological means of binding and neutralizing endotoxin effectively. We hypothesized that enhancement of triacylglycerol-rich lipoproteins via high-fat enteral nutrition would reduce endotoxemia and prevent bacterial translocation.
A rat model of nonlethal hemorrhagic shock was used. Hemorrhagic shock (HS) rats were divided into 3 groups: rats starved overnight (HS-S); rats fed with a low-fat enteral diet (HS-LF), and rats receiving a high-fat enteral diet (HS-HF).
Circulating triacylglycerol and apolipoprotein B, reflecting the amount of triacylglycerol-rich lipoproteins, were elevated in HS-HF rats compared with both HS-S rats (P <or= 0.005 and P <or= 0.05, respectively) and HS-LF rats (P <or= 0.005 and P <or= 0.05). Circulating endotoxin was lower in HS-HF rats (7.2 +/- 10.2 pg/ml) compared with both HS-S rats (29.1 +/- 13.4 pg/ml, P <or= 0.005) and HS-LF rats (29.9 +/- 5.2 pg/ml, P <or= 0.005). In line, bacterial translocation was lower in HS-HF rats (incidence 4/8 rats; median 3 [range 0-144] cfu/g) compared with both HS-S rats (8/8; 212 [60-483] cfu/g; P = 0.006), and HS-LF rats (8/8; 86 [30-209] cfu/g; P = 0.002).
This study is the first to show that high-fat enteral nutrition, leading to increased plasma triacylglycerol and apolipoprotein B levels, significantly decreases endotoxemia and bacterial translocation after hemorrhage.
确定通过高脂肠内营养潜在增强内毒素中和作用是否会影响出血后的内毒素血症和细菌移位。
由于肠屏障功能衰竭导致的内毒素和细菌移位是出血后脓毒症发病机制中的重要起始事件。全身抑制内毒素活性可减轻细菌移位和远处器官损伤。富含三酰甘油的脂蛋白构成了有效结合和中和内毒素的生理方式。我们假设通过高脂肠内营养增强富含三酰甘油的脂蛋白会降低内毒素血症并预防细菌移位。
采用非致死性失血性休克大鼠模型。失血性休克(HS)大鼠分为3组:禁食过夜的大鼠(HS-S);喂食低脂肠内饮食的大鼠(HS-LF),以及接受高脂肠内饮食的大鼠(HS-HF)。
与HS-S大鼠(分别为P≤0.005和P≤0.05)和HS-LF大鼠(分别为P≤0.005和P≤0.05)相比,反映富含三酰甘油脂蛋白量的循环三酰甘油和载脂蛋白B在HS-HF大鼠中升高。与HS-S大鼠(29.1±13.4 pg/ml,P≤0.005)和HS-LF大鼠(29.9±5.2 pg/ml,P≤0.005)相比,HS-HF大鼠的循环内毒素较低(7.2±10.2 pg/ml)。同样,与HS-S大鼠(8/8;212[60 - 483] cfu/g;P = 0.006)和HS-LF大鼠(8/8;86[30 - 209] cfu/g;P = 0.002)相比,HS-HF大鼠的细菌移位较低(发生率4/8只大鼠;中位数3[范围0 - 144] cfu/g)。
本研究首次表明,导致血浆三酰甘油和载脂蛋白B水平升高的高脂肠内营养可显著降低出血后的内毒素血症和细菌移位。