Pretreatment with high-fat enteral nutrition reduces endotoxin and tumor necrosis factor-α and preserves gut barrier function early after hemorrhagic shock
Pretreatment with high-fat enteral nutrition reduces endotoxin and tumor necrosis factor-α and preserves gut barrier function early after hemorrhagic shock
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DOI：
10.1097/01.shk.0000101671.49265.cf
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发表时间：
2004-01-01
期刊：
影响因子：
3.1
通讯作者：
Greve, JWM
中科院分区：
文献类型：
--
作者：
Luyer, MDP;Buurman, WA;Greve, JWM
革兰氏阴性脓毒症是一种潜在的致命性临床综合征，其特征是对细菌(Endo)毒素的促炎反应(肿瘤坏死因子-α)和肠道屏障功能丧失。最近，我们发现高脂肪肠内营养对失血性休克大鼠的迟发性细菌易位有保护作用。然而，这种保护的基础尚不清楚。我们假设，观察到的保护作用是早期抑制内毒素和随后的炎症反应导致保留肠道屏障功能的结果。将SD大鼠分为饥饿过夜组(HS-S)、低脂饲料组(HS-LF)和高脂饲料组(HS-HF)，然后进行非致死性失血性休克。失血90min后，HS-HF大鼠动脉内毒素水平(4.0+/-0.6pg/m L)显著低于HS-LF(10.7+/-0.9pg/m L，P=0.002)和HS-S(15.2+/-2.2pg/m L，P=0.001)。有趣的是，HS-HF大鼠动脉肿瘤坏死因子-α水平(17.9±10.4pg/mL)也低于HS-LF(83.5±16.7pg/mL，P<0.01)和HS-S大鼠(180.9+/-67.9pg/mL，P<0.02)。HS-HF可防止失血性休克大鼠回肠和结肠紧密连接结构(ZO-1)丢失。同时，HS-HF大鼠的肠屏障功能得到保护，表现为对辣根过氧化物酶的通透性降低(P<；0.05)，细菌侵袭减少，失血性休克后早期细菌移位减少10倍。本报告描述了一种从营养上预防失血性休克后内毒素血症、随后的炎症反应和肠道屏障衰竭的新策略。高脂肪肠内营养需要进一步评估，作为一种干预措施，以防止有脓毒症风险的患者发生潜在的致命全身炎症反应。
Gram-negative sepsis is a potentially fatal clinical syndrome characterized by a proinflammatory response (tumor necrosis factor-alpha) to bacterial (endo)toxins and gut barrier function loss. Recently, we found that high-fat enteral nutrition protects against late bacterial translocation in a model of hemorrhagic shock in rats. However, the basis for this protection is unknown. We hypothesized that the observed protection is the result of an early inhibition of endotoxin and the subsequent inflammatory response resulting in a preserved gut barrier function. Sprague-Dawley rats were divided into a group that was starved overnight (HS-S), fed with a low-fat enteral diet (HS-LF) or fed wih a high-fat enteral diet (HS-HF), and subsequently subjected to a nonlethal hemorrhagic shock. Ninety minutes after hemorrhage, arterial endotoxin significantly decreased in HS-HF rats (4.0 +/- 0.6 pg/mL) compared with HS-LF rats (10.7 +/- 0.9 pg/mL, P = 0.002) and HS-S rats (15.2 +/- 2.2 pg/mL P = 0.001). Interestingly, arterial tumor necrosis factor-a was also decreased in HS-HF rats (17.9 +/- 10.4 pg/mL) compared with HS-LF (83.5 +/- 16.7 pg/mL, P < 0.01) and HS-S rats (180.9 +/- 67.9 pg/mL, P < 0.02). Loss of tight junction structure (ZO-1) observed in ileum and colon of control hemorrhagic shock rats was prevented in HS-HF rats. In parallel, intestinal barrier function was preserved in HS-HF rats, evidenced by a reduced permeability to horseradish peroxidase (P < 0.05), less bacterial invasion, and a 10-fold reduction of bacterial translocation early after hemorrhagic shock. This report describes a new strategy to nutritionally prevent endotoxemia, the subsequent inflammatory response and gut barrier failure following hemorrhagic shock. High-fat enteral nutrition requires further evaluation as an intervention to prevent a potentially fatal systemic inflammatory response in patients at risk for sepsis.