The effect of N-acetylcysteine on oxidative stress in intestine and bacterial translocation after thermal injury

Ischemia due to transient splanchnic vasoconstriction following major burns causes oxidative and/or nitrosative damage in intestinal tissue followed by reperfusion injury. Thus, burn injury leads to breakdown in the intestinal mucosal barrier which can induce bacterial translocation (BT). As an antioxidant and anti-inflammatory agent the protective effects of N-acetylcysteine (NAC) are documented in several studies. This study was designed to determine the effect of NAC treatment on the oxidative stress in the intestine and BT after burn injury. To evaluate this, 32 Wistar rats were randomly divided into four groups as sham (n = 8), burn (n = 8), pre-burn, NAC injection (150 mg kg⁻¹, intraperitoneally) 15 min before thermal injury (n = 8), post-burn, NAC injection (150 mg kg⁻¹, intraperitoneally) 2 h after thermal injury. Under anesthesia, the shaved dorsal skin of rats was exposed to boiling water for 12 s to induce burn injury in a standardized manner. Twenty-four hours later, tissue samples from mesenteric lymph nodes (MLN), spleen, and liver were obtained under sterile conditions for microbiological analysis and ileum samples were harvested for biochemical analysis. In the burn group, the incidence of isolating bacteria in MLN, spleen, and liver specimens was significantly higher than other groups. NAC treatment prevented burn-induced BT in both pre- and post-burn groups. Thermal injury caused a significant decrease in glutathione (GSH) level, significant increases in malondialdehyde (MDA) and myeloperoxidase (MPO) activity at post-burn 24th hour. Treatment of rats with NAC significantly elevated the reduced GSH levels while decreasing MDA levels and MPO activity. These data suggested that NAC has a crucial cytoprotective role in intestinal mucosal barrier and preventive effects against burn injury-induced BT.     

The effect of ethyl pyruvate on oxidative stress in intestine and bacterial translocation after thermal injury

BACKGROUND: Thermal injury causes a breakdown in the intestinal mucosal barrier due to ischemia reperfusion injury, which can induce bacterial translocation (BT), sepsis, and multiple organ failure in burn patients. The aim of this study was to investigate the effect of ethyl pyruvate (EP) on intestinal oxidant damage and BT in burn injury. MATERIALS AND METHODS: Thirty-two rats were randomly divided into four groups. The sham group was exposed to 21 degrees C water and injected intraperitoneal with saline (1 mL/100 g). The sham + EP group received EP (40 mg/kg) intraperitoneally 6 h after the sham procedure. The burn group was exposed to thermal injury and given intraperitoneal saline injection (1 mL/100 g). The burn + EP group received EP (40 mg/kg) intraperitoneally 6 h after thermal injury. Twenty-four hours later, tissue samples were obtained from mesenteric lymph nodes, spleen, and liver for microbiological analysis and ileum samples were harvested for biochemical analysis. RESULTS: Thermal injury caused severe BT in burn group. EP supplementation decreased BT in mesenteric lymph nodes and spleen in the burn + EP group compared with the burn group (P < 0.05). Also, burn caused BT in liver, but this finding was not statistically significant among all groups. Thermal injury caused a statistically significant increase in malondialdehyde and myeloperoxidase levels, and EP prevented this effects in the burn + EP group compared with the burn group (P < 0.05). CONCLUSION: Our data suggested that EP can inhibit the BT and myeloperoxidase and malondialdehyde production in intestine following thermal injury, suggesting anti-inflammatory and anti-oxidant properties of EP.     

Reversal of the effect of albumin on gut barrier function in burn by the inhibition of inducible isoform of nitric oxide synthase

HYPOTHESIS: The use of albumin in the early resuscitation formula after major burn has been forbidden because of its damaging effect on the gut barrier function. We hypothesize that inhibition of the inducible isoform of nitric oxide synthase to stabilize endothelial permeability and to retain albumin in the vascular space will ameliorate the major trauma-induced gut barrier dysfunction. DESIGN, INTERVENTIONS, AND MAIN OUTCOME MEASURES: In experiment 1, specific pathogen-free rats undergoing 35% total body surface area burn or sham burn were given equal volumes (7.5 mL/kg) of isotonic sodium chloride solution or albumin from femoral veins for fluid resuscitation at 0, 4, or 8 hours after burn. In experiment 2, intraperitoneal S-methylisothiourea sulfate (7.5 mg/kg) was given immediately after burn to rats from different groups, as in experiment 1 (SMT groups). At 24 hours after burn, the intestinal mucosa was assayed for myeloperoxidase activity as an index for neutrophil sequestration, the distribution of fluorescein isothiocyanate-dextran across the lumen of small intestine was determined to evaluate the intestinal permeability, and bacterial translocation (BT) to the mesenteric lymph nodes (MLNs) and histological findings in the ileum were also examined. RESULTS: Compared with sham burn, burn induced significant increases in intestinal mucosa myeloperoxidase activity, intestinal permeability, BT to the MLNs, and villi sloughing in rats. Albumin administration at 0 or 4 hours after burn enhanced the increases in neutrophil sequestration, permeability, and villi sloughing compared with saline injection at the same times. In contrast, injection of albumin in the burn-SMT group did not aggravate these changes in intestinal myeloperoxidase activity, intestinal permeability, BT to the MLNs, and villi edema. Burn-SMT rats with albumin injections at 4 or 8 hours after burn showed significant 35% and 52% decreases, respectively, in intestinal permeability compared with burn-SMT-saline rats. Use of albumin at 8 hours after burn in combination with S-methylisothiourea significantly attenuated BT to the MLNs and reduced villi edema. CONCLUSIONS: Early albumin resuscitation aggravated the burn-induced gut damage. Albumin administration and inhibition of the inducible isoform of nitric oxide synthase in combination decreased burn-induced gut barrier dysfunction and reversed the damaging effect of albumin on gut barrier function and decreased BT.     

烧伤大鼠小肠肌间神经丛中一氧化氮合酶的组织化学研究

目的　探讨烧伤后大鼠小肠壁内一氧化氮合酶 (NOS)的活性及分布的变化规律。　方法　采用NADPH -黄递酶 (NDP)组织化学法和整装铺片技术对烧伤大鼠小肠壁内NOS的活性及分布进行定量和定位研究。　结果　NOS广泛分布于大鼠小肠壁内 ,主要定位于肌间神经丛。NOS阳性神经元多为圆形和卵圆形 ,神经纤维中多含有膨体 ,形成“串珠”样结构 ,且多与血管和肌纤维伴行。烧伤后肌间神经丛中NOS阳性神经元密度变化不显著 (P >0 .0 5 ) ,但神经元内NOS活性则显著下降(P <0 .0 5～ 0 .0 1) ,同时发现烧伤后NOS阳性神经元结构模糊 ,神经纤维断裂较多 ,未能形成完整的神经纤维网 ,神经纤维中NOS阳性膨体亦明显减少。结论　烧伤后大鼠小肠肌间神经丛中NOS阳性神经结构受损 ,神经元内NOS活性下降 ,同时一氧化氮 (NO)的释放途径亦存在障碍 ,这些变化可能与烧伤后肠道结构受损 ,功能障碍密切相关     

Differential pathophysiology of bacterial translocation after thermal injury and sepsis.

Bacterial translocation (BT) occurs transiently after thermal injury and may result from an ischemic intestinal insult. To evaluate continued intestinal ischemia in the ongoing BT associated with sepsis after injury, rats were randomized to (1) 30% burn injury with Pseudomonas wound infection (BI), (2) BI + fluid resuscitation (BI + Fluid), (3) BI after allopurinol pretreatment to inhibit xanthine oxidase (BI + Allo), or (4) BI after azapropazone pretreatment to inhibit neutrophil degranulation (BI + Aza). On postburn days (PBD) 1, 4, and 7, animals were studied for evidence of BT and intestinal lipid peroxidation. BI + Fluid, BI + Allo, and BI + Aza significantly (p less than 0.05) reduced rates of BT and ileal lipid peroxidation acutely after thermal injury (PBD 1) compared to BI. All four groups had equally high rates of BT associated with the onset of sepsis (PBDs 4 and 7), without evidence of further intestinal lipid peroxidation. These data indicate that the chronic gut barrier failure associated with sepsis after injury occurs independently of continued intestinal ischemia.     

烧伤后肠黏膜细胞外基质与细胞凋亡关系的实验研究

目的　探讨烧伤后大鼠肠黏膜细胞凋亡与细胞外基质的关系。　方法　 30只Wistar大鼠随机分为烧伤后 6、12h,1、3、5d组及正常对照组 ,每组 5只。检测肠黏膜上皮细胞凋亡数、cas pases 3酶活性、细胞外基质成分 (层粘连蛋白、Ⅳ型胶原 )含量 ,并作相关分析。　 结果　烧伤后大鼠肠上皮凋亡细胞数、caspases 3的活性较正常对照组明显升高 (P <0.0 5或 0 .0 1) ,大鼠肠黏膜层粘连蛋白、Ⅳ型胶原含量较正常对照组下降 ( P <0.0 5或 0 .0 1)。直线相关分析结果 :烧伤后肠黏膜层粘连蛋白、Ⅳ型胶原含量变化与细胞凋亡数呈显著的负相关 (r =- 0.5 75, - 0.6 13,P <0 0 5 )。　 结论　烧伤后大鼠肠黏膜细胞凋亡增加 ,且与细胞外基质的变化相关。     

早期肠道喂养改善烧伤后肠道血液灌流的实验研究

目的 探讨早期肠道喂养改善烧伤大鼠肠血液灌流的机理。方法 采用３０％体表面积Ⅲ度烧伤大鼠模型,分为正常对照（Ｃ）、单纯烧伤（Ｂ）和早期喂养（ＶＩＰ）含量及肠粘膜血流量（ＬＭＢＦ）。结果 烧伤后肠组织中ＥＴ、ＮＯ、ＶＩＰ及ＥＴ／ＶＩＰ比值均呈上升趋势,而ＩＭＢＦ则显著低于伤前。ＥＦ组中ＥＴ含量及ＥＴ／ＮＯ、ＥＴ／ＶＩＰ比值明显低于Ｂ组,而ＮＯ、ＶＩＰ及ＩＭＢＦ则高于Ｂ组,肠道喂养烧伤后肠道缺血状况的     

烧伤早期营养对大鼠降钙素基因相关肽影响的实验研究

目的观察烧伤早期不同营养途径对肠道的复苏效应,及其与降钙素基因相关肽(cal-citoningene-relatedpeptide,CGRP)的关系方法30%TBSAⅢ度烧伤Wistar大鼠,随机分为灌喂组(EF组,30只)及早期静脉营养组(EPN组,30只).此外,6只大鼠不烧伤,作对照组(C组).伤后6、12、24、48、72h观察大鼠一般情况、肠黏膜血流量、血浆CGRP免疫活性物质浓度、CGRP染色阳性物质在肠道的变化.结果烧伤后大鼠肠黏膜血流量下降,EF组下降程度明显低于EPN组(P＜0.05～0.01);烧伤后血浆CGRP升高,EF组血浆CGRP在伤后72h明显低于EPN组(P＜0.01);肠道CGRP阳性染色物质在烧伤后明显减少(P＜0.05～0.01),EF组在伤后24、48h明显多于EPN组(P＜0.05);肠黏膜血流量下降和肠肌间丛CGRP下降呈正相关(r=0.72,P＜0.05).结论肠道营养在烧伤早期肠道的复苏效应方面较静脉营养优越,伤后肠道CGRP免疫活性物质减少,血浆CGRP免疫活性物质过度增高可能是烧伤后肠道血供减少的重要机制之一,早期肠道营养可能通过调节CGRP而发挥复苏作用.     

富含精氨酸早期肠内营养对烧伤后肠黏膜增殖的实验研究

目的研究富含精氨酸的肠内营养对大鼠烧伤后肠道黏膜上皮增殖的影响.方法观察富含精氨酸早期肠内营养组(AEF组)、单纯早期肠内营养组(EF组)及延迟肠内营养(DF组)大鼠在烧伤后第1、3、6和9d时,肠黏膜增殖细胞核抗原标记指数(PCNALI)和肠黏膜脱氧核糖核酸(DNA)的变化.结果在烧伤后第1天,各组肠道黏膜PCNA的阳性细胞极为罕见.与DF组相比,在烧伤后第3天AEF组肠黏膜PCNALI即有明显升高[(20.61±7.53)‰vs(6.9±2.7)‰,P＜0.05),而EF组在烧伤后第6天才有显著升高(18.2±5.1)‰vs(10.81±5.10)‰P＜0.05].结论烧伤后肠黏膜屏障受损,肠上皮细胞增殖受抑.单纯早期肠道可减轻肠黏膜损害,但不能尽快改善肠道黏膜增殖.通过在早期肠道营养中加用精氨酸可进一步增加肠道黏膜上皮的增殖.     

重视烧伤后肠道紧密连接屏障功能障碍的研究

Severe burn injury is often accompanied by intestinal epithelial tight junction barrier dysfunction, which is believed to be closely associated with postburn shock, inflammation, hypermetabolism, infection, organ dysfunction etc. Recent studies have documented the critical role of tight junction-associated protein regulation in intestinal epithelial barrier dysfunction induced by severe burn injury. Myosin light chain (MLC) phosphorylation regulated by both myosin light chain kinase, which can phosphorylate MLC directly, and Rho-associated kinase,which can inhibit MLC phosphatase and then induce MLC phosphorylation indirectly, play a critical role in intestinal epithelial tight junction barrier dysfunction which occurs in severe burn injury. Recent advances have provided new insights into the mechanisms and the therapeutic strategies of intestinal epithelial tight junction barrier dysfunction following severe burn injury.     

大鼠烫伤早期肠黏膜组织热休克蛋白HSP70和HSP90的表达

目的 研究烧伤早期肠黏膜组织热休克蛋白HSP70和HSP90的表达、组织含量和分布的变化规律,探讨烧伤早期肠黏膜组织细胞的热休克反应在机体的病理生理反应中的意义。方法 以烫伤大鼠为模型,利用ELISA、免疫印迹分析和免疫组织化学方法,分析和研究肠黏膜组织HSP70和HSP90的表达、组织含量和分布及其功能状态。结果 (1)大鼠烫伤早期肠黏膜游离HSP70的含量有非常显的短暂降低;(2)肠黏膜组织HSP70和HSP90的总体含量在烧伤后有显升高;(3)烧伤早期肠黏膜组织HSP70的分子结构存在显的不均一性。结论 肠黏膜组织细胞中两种热休克蛋白表达、含量和分布的规律性变化,在肠黏膜组织细胞的应激反应、进而在肠道的黏膜屏障机制中,可能有重要的意义。     

休克期切痂对血浆内皮素及NO水平的影响

目的观察烧伤休克期切痂和休克期后切痂对血浆内皮素及一氧化氮水平的影响。方法利用小型猪制成35％Ⅲ度烧伤动物模型,分为两组,休克期切痂组(S组)于伤后24小时切痂,对照组(C组)于伤后96小时切痂,分别检测血浆内皮素(ET)、一氧化氮(NO),并计算ET/NO。结果两组ET及NO均高于伤前,伤后96小时开始S组ET明显低于C组;而NO水平S组明显高于C组;ET/NO亦显示伤后24小时开始S组明显低于C组。结论休克期切痂可减轻内皮细胞损伤,减轻渗出与水肿,减少组织缺氧,改善微循环。     

烧伤后肠相关淋巴组织调控因子基因表达与IgA浆细胞变化

目的 观察烧伤后局部肠相关淋巴组织IL-4、IL-6与IgA浆细胞变化的关系。方法 125只SPF小鼠分为正常对照组(A)、给菌组(B)及给菌后烧伤组(C);B、C组动物经口给入白色念珠菌,C组在给菌后14d致以20％TBSAⅢ。烧伤,伤后1、2、3d活杀取材。进行白色念珠菌粘附肠粘膜计数;计数肠固有层IgA浆细胞;观察IL-4、IL-6表达。结果 1、伤后潘氏结中IL-4表达下降、而肠固有层IL-6水平高于伤前。2．伤后IgA浆细胞数量明显减少、而白色念珠菌粘附明显增加。结论 烧伤后潘氏结中IL-4表达减少造成IgA型浆细胞减少。导致白色念珠菌粘附增加。     

The effects of ketamine and propofol on bacterial translocation in rats after burn injury

BACKGROUND: Bacterial translocation (BT) occurs after thermal injury and may result from an ischemic intestinal insult. The aim of the study was to investigate the effects of ketamine and propofol as anesthetic agents on BT in an animal model of burn injury. METHODS: Sixty male Wistar Albino rats were randomly assigned to six groups of 10 rats each. Anesthesia was induced and maintained with ketamine in groups 1, 2 and 3 and with propofol in groups 4, 5 and 6 during 6 h. Groups 2, 3, 5 and 6 received 30% total body surface area (TBSA) third-degree burns. Groups 1 and 4 had no burn injury. Then, they were allowed to recover from the anesthesia at the end of 6 h. Mean arterial pressure (MAP) was monitored continuously and maintained within 10% of baseline (before burn injury) levels in all animals. Animals in groups 3 and 6 had a laparotomy to obtain a tissue sample from the terminal ileum for determination of intestinal lipid peroxidation by-product malondialdehyde (MDA) before (baseline) and 6 and 24 h after burn injury (ABI). So these animals were not included in the BT studies. At postburn 24 h, animals in groups 1, 2 and 4, 5 were sacrified and samples were taken from the mesenteric lymph nodes (MLN), liver and spleen for bacteriologic cultures. RESULTS: The incidence of BT was found to be significantly higher in group 2 than in all the other groups. Bacterial translocation incidence of group 5 was not significantly different from that of groups 4 and 1. Group 5 was associated with a significantly reduced number of enteric organisms per gram of tissue compared to group 2. Baseline MDA contents of groups 3 and 6 were similar. Ileal MDA levels were increased in group 3, but there were no significant changes in group 6 at 6 and 24 h ABI compared to baseline. CONCLUSION: Our results suggest that propofol as an anesthetic agent may prevent BT by scavenging reactive oxygen species and inhibiting lipid peroxidation in an animal model of burn injury.     

休克期切痂对血浆内皮素及NO水平的影响

目的观察烧伤休克期切痂和休克期后切痂对血浆内皮素及一氧化氮水平的影响。方法利用小型猪制成３５％Ⅲ度烧伤动物模型，分为两组，休克期切痂组（Ｓ组）于伤后２４小时切痂，对照组（Ｃ组）于伤后９６小时切痂，分别检测血浆内皮素（ＥＴ）、一氧化氮（ＮＯ），并计算ＥＴ／ＮＯ。结果两组ＥＴ及ＮＯ均高于伤前，伤后９６小时开始Ｓ组ＥＴ明显低于Ｃ组；而ＮＯ水平Ｓ组明显高于Ｃ组；ＥＴ／ＮＯ亦显示伤后２４小时开始Ｓ组明显低于Ｃ组。结论休克期切痂可减轻内皮细胞损伤，减轻渗出与水肿，减少组织缺氧，改善微循环     

早期肠道喂养对烧伤大鼠肠道一氧化氮合酶的影响

目的阐明烧伤大鼠经早期肠道喂养后肠组织中一氧化氮合酶(NOS)的变化规律及其与肠粘膜血流量(IMBF)的关系。方法采用30％TBSAⅢ度烧伤大鼠模型,分为正常对照(C)组,单纯烧伤(B)组和早期喂养(EF)组,分别检测伤前及伤后0,3,6,12,24,48小时肠组织中 NOS 活性,包括原生型 NOS(cNOS)和诱导型 NOS(iNOS),并测定肠粘膜血流量。结果烧伤后各组 cNOS 和 IMBF 呈下降趋势,二者呈显著正相关(r=0.97,P<0.01),而 NOS 总活性和 iNOS 活性都呈上升趋势,IMBF 与 iN-OS 和总 NOS 相关不显著。烧伤后 EF 组 cNOS 和 IMBF 明显高于 B 组,iNOS 则低于 B 组,NOS 总活力两组无显著差异。结论①两型 NOS 中 cNOS 与 IMBF 的关系更加密切。②早期肠道喂养改善烧伤后肠道缺血状况,可能与食物对肠壁神经的刺激从而提高 cNOS 活性有关。     

严重烧伤后糖皮质激素受体变化在应激性胃粘膜损害中的作用

目的　探讨糖皮质激素受体变化在烧伤后应激性胃粘膜损害中的作用。　方法　观察大鼠严重烧伤后不同时相胃粘膜组织糖皮质激素受体的动态变化及胃粘膜损伤情况。　结果　伤后6h皮质醇含量明显升高 ,12h达高峰 (P <0 .0 5～ 0 .0 1) ,而胃粘膜细胞胞浆内糖皮质激素受体水平显著下降 (P <0 .0 5～ 0 .0 1) ,胃粘膜损伤指数于伤后 6、12、2 4、4 8h显著增加 (P <0 .0 5～ 0 .0 1)。　结论　严重烧伤后糖皮质激素受体减少是应激性胃粘膜损害的重要因素     

Inhibition of nitric oxide synthase reverses the effect of albumin on lung damage in burn

BACKGROUND: Early colloid resuscitation in major burn patients has been stopped because of its deteriorating effect on thermal injury-induced vascular hyperpermeability. We hypothesized that inhibition of inducible nitric oxide synthase (iNOS) to stabilize endothelial permeability and to retain colloid solution in the vascular space will reverse its effect on lung damage. STUDY DESIGN: In experiment 1, specific pathogen free rats underwent 35% total-body surface area burn or sham burn and were given equal volumes (7.5 mL/kg) of normal saline or albumin from femoral veins for fluid resuscitation immediately after burn. In experiment 2, S-methylisothiourea (SMT, 7.5 mg/kg, IP) was given immediately after burn to rats from different groups, as in experiment 1. At 8 hours after burn, blood was assayed for peroxynitrite-mediated dihydrorhodamine 123 (DHR 123) oxidation, and lung tissues were harvested for myeloperoxidase (MPO) determination and histologic studies. Pulmonary microvascular dysfunction was quantified by measuring the extravasations of Evans blue dye. RESULTS: Blood peroxynitrite level and iNOS expression, MPO activity, permeability, and inflammatory cell infiltration of lungs were significantly induced after thermal injury. Albumin resuscitation after burn without iNOS inhibition enhanced thermal injury-induced lung damage with 10%, 14%, and 5% increases in blood DHR oxidation level, lung MPO activity, and lung permeability, respectively, compared with saline injection. In contrast, burn + SMT rats with albumin injection showed significant, 23%, 37%, and 20%, decreases, respectively, in blood DHR 123 oxidation level, lung MPO activity, and lung permeability compared with burn + SMT + saline rats. CONCLUSIONS: Thermal injury induced lung damage. Restoration of extracellular fluid in early burn shock with albumin markedly augmented the lung neutrophil deposition, lung permeability increase, and blood peroxynitrite level. Inhibition of iNOS before albumin supplementation reversed its damaging effects on thermal injury-induced lung dysfunction to beneficial ones.     

Burn-induced transcriptional regulation of small intestinal ornithine decarboxylase.

The mechanisms responsible for gut repair after burn injury have not been established. Polyamines are required for eukaryotic cell growth and differentiation. The enzyme ornithine decarboxylase (ODC) catalyzes the rate-limiting step in polyamine biosynthesis. The role of ODC activity in repair of injured small bowel mucosa after burns has not been investigated. This study examined the effects of burn injury on gut mucosal mass and regulation of ODC gene expression and ODC activity in small bowel mucosa. After an overnight fast, 18 male Sprague-Dawley rats (250 to 300 g) were randomized into sham, 20% burn, or 60% burn groups. We measured ODC activity, mucosal weight, deoxyribonucleic acid (DNA) content, and protein content in proximal and distal small bowel mucosa at postburn intervals of 0, 3, 12, 24, and 48 hours. Gut mucosal ODC messenger ribonucleic acid (mRNA) levels were determined. Burn injury caused significant atrophy of the gut mucosa by 12 hours postburn; restoration was evident by 48 hours after burn. ODC activity was increased in the proximal small bowel at 12 and 24 hours after burn in the rats in both the 20% burn and 60% burn groups; by contrast, only rats in the 60% burn group had increased ODC activity in the distal small bowel. ODC mRNA levels increased in the proximal gut mucosa as early as 3 hours after the burn and returned to control values after 24 hours. These data show that mucosal restoration begins soon after burn injury and that the induction of ODC mRNA and ODC activity are important events.     

早期肠道喂养对烧伤大鼠肠道一氧化氮合酶的影响

OBJECTIVE: Our previous studies have proved that early enteral feeding could improve intestine blood flow after burn injury. But the mechanism was far from being clarified. This study was attempted to explore the effects of early enteral feeding on nitric oxide synthase (NOS) activity in burned rat small intestine and the relationship between the intestine mucosa blood flow (IMBF) and the activity of NOS. METHODS: The rats were randomly divided into three groups: burned control (B), burned and early enteral feeding (EF), and normal control (C). The activity of NOS including constitute NOS(cNOS) and inducible NOS(iNOS), and the IMBF were determined at postburn 0, 3, 6, 12, 24, 48 hours. RESULTS: It was found that cNOS activity and IMBF were decreased markedly postburn, and there was positive correlation between cNOS and IMBF (r = 0.97, P < 0.01). But the activity of iNOS, total NOS were increased significantly postburn, they had no correlation to the IMBF. In EF group cNOS activity and the IMBF were significantly higher, the iNOS was obviously lower than that of B group and there was no significant difference of total activity of NOS between two groups. CONCLUSION: Our results suggested that NOS which is catalyzed from cNOS may play main role in adjusting IMBF. By using early enteral feeding the activity of cNOS is increased and the ischemic state in small intestine is improved after burn injury.