早期手术对烧伤大鼠肝血流量的影响

目的通过测定 TBSA30％Ⅲ度烧伤大鼠早期手术后肝血流量的变化,了解早期手术对肝脏血液灌流的影响。方法 Wistar 雄性大鼠34只,分为4组:烧伤组(A 组),输液组(B 组),早期手术组(C 组),正常对照组(D 组)。输液组经股静脉插管输入乳酸林格氏液;早期手术组于立即补液的同时行切痂同种异体植皮术。各组于伤后0,0.5,1,2,3,6,12和24小时,应用氢清除法测定肝血流量。结果 A 组与 B 组伤后均出现肝血流量显著下降,B 组直至伤后24小时肝血流量才恢复正常,而 C 组伤后肝血流量保持相对稳定,与正常对照组比较无显著意义。结论严重烧伤后立即液体复苏尚不足以维持有效的肝脏血流灌流,烧伤后早期手术尽早地去除焦痂组织,对改善肝血流量具有重要作用。     

The effects of early excision and grafting on myocardial inflammation and function after burn injury

BACKGROUND: Sepsis is a frequent complication of burn injury despite absence of confirmed infection. Numerous investigators have proposed that the burn wound itself is a primary stimulus for postburn inflammation, and that early excision of the burn wound attenuates the hypermetabolic and inflammatory responses to burn injury. However, others have suggested that aggressive fluid resuscitation and correction of postburn fluid and electrolyte deficits should be the primary focus of intervention in the first 24 hours postburn. This present study determined whether excision and grafting of the burned wound within 30 minutes after injury abrogated myocardial inflammation and contractile defects that occur after burn injury. METHODS: In group 1, Sprague Dawley rats were given a third-degree burn over 20% total body surface area (TBSA), whereas rats in group 2 had burns over 30% TBSA and no wound excision. Rats in groups 3 and 4 had burn over 20% and 30% TBSA, respectively, followed by-wound excision and grafting (WE/G) within 30 minutes after completing burn injury. Group 5 included sham burn with no excision, whereas rats in groups 6 and 7 included shams that had either 20% or 30% normal skin excised and grafted to provide appropriate surgical controls. All rats received lactated Ringer's (4 mL/kg/% burn or percent wound excision). Twenty-four hours postburn, hearts were perfused (Langendorff) to assess ventricular function; myocytes were isolated to examine cytokine secretion and Ca2+/Na+ homeostasis. RESULTS: Burn in the absence of wound excision produced myocardial inflammation and contractile defects as indicted by a lower left ventricular pressure and lower rate of left ventricular pressure rise (+dP/dt) and fall (-dP/dt) response to maximal increases in preload or perfusate Ca2+ compared with responses measured in sham hearts. WE/G within 30 minutes after burn injury reduced myocyte secretion of proinflammatory cytokines and improved left ventricular pressure and +/-dP/dt responses to inotropic challenge. CONCLUSION: Cutaneous burn injury and the loss of the skin barrier function contribute, in part, to the myocardial inflammation which, in turn, contributes to myocardial contractile dysfunction that is characteristic of major burn injury.     

Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury

This study tested the hypothesis that nitric oxide (NO) synthesized from inducible NO synthase (iNOS) is responsible for the cardiac dysfunction observed after burn and smoke inhalation injury. Twelve sheep received 40% third-degree burn and smoke inhalation under halothane anesthesia. The animals were divided into two groups: a MEG group [iNOS was inhibited with mercaptoethylguanidine (MEG), a selective inhibitor of iNOS, n=6] and a control group (n=6). The control group showed a significant increase in NO₂⁻/NO₃⁻ (NO_x) concentration, metabolite of NO, in plasma after 24 h, whereas the MEG group did not. In the control group, cardiac depression was observed immediately after injury associated with hemoconcentration. Cardiac function returned to a normal level within 6 h following injury. In the control group cardiac dysfunction was observed again after 24 h although the hemoconcentration peaked at 24 h after injury and then began to resolve. In the MEG group, cardiac depression and hemoconcentration were not observed. The present data suggest that cardiac depression seen with this combination injury consists of two phases and that the later phase is mediated by iNOS–NO.     

Modulation of inflammatory and catabolic responses in severely burned children by early burn wound excision in the first 24 hours

HYPOTHESIS: Early burn wound excision modulates the hypermetabolic response in severe pediatric burn injuries. DESIGN: Before-after trial. SETTING: A 30-bed burn referral center in a private, university-affiliated hospital. METHODS: We studied 35 severely burned children who were divided into 2 groups. One group (n = 20) was treated with early burn wound excision within 24 hours after the injury. The second group (n = 15) was treated conservatively with silver sulfadiazine in other burn facilities for 5 days, and burn wounds were surgically excised when patients were admitted to our burn center on day 6 after the injury. Data compiled included oxygen consumption and acute-phase protein, interleukin 1beta; interleukin 6, interleukin 10, tumor necrosis factor alpha, and anabolic hormone (growth hormone, insulinlike growth factor type 1) levels preoperatively and 24 hours and 5 days postoperatively. MAIN OUTCOME MEASURES: Acute-phase and hypermetabolic responses. RESULTS: Early burn wound excision abrogated the hypermetabolic response in pediatric burn patients. Patients who underwent conservative treatment had a significantly more severe inflammatory and hypermetabolic response at the same time interval and significantly lower levels of anabolic hormones. CONCLUSIONS: Early burn wound excision is a safe therapeutic approach that modulates the hypermetabolic response after burn injury. It was superior to the conservative treatment of silver sulfadiazine and delayed excision, and it should be considered when treating all severe full-thickness burns.     

严重烧伤抗休克对胃肠粘膜内缺血的研究

探讨烧伤早期胃肠缺血的发生规律。方法采用模拟临床的ＴＢＳＡ３０％Ⅲ度烧伤小型模型，从血流动力学、胃肠缺血、血液流学等方面探讨烧伤早期胃肠缺血的发生规律及相关因素。     

The role of poly(ADP-ribose) synthetase inhibition on the intestinal mucosal barrier after thermal injury

Oxidative and nitrosative stressor agents can trigger DNA strand breakage, which then activates the nuclear enzyme poly(ADP-ribose) synthetase (PARS). Activation of the enzyme depletes the intracellular concentration of energetic substrates such as nicotinamide adenine dinucleotide (NAD). This process can result in cell dysfunction and cell death. PARS inhibitors have been successfully used in ischemia–reperfusion injury, inflammation and sepsis in several experimental models. In our experimental study, we investigated the role of 3-aminobeanzamide (3-AB), a non-specific PARS inhibitor, on the intestinal mucosal barrier after burn injury. Twenty-four Wistar rats were randomly divided into three groups. The sham group (n = 8) was exposed to 21 °C water while the burn group (n = 8) and the burn + 3-AB group (n = 9) were exposed to boiling water for 12 s to produce a full thickness burn in 35–40% of total body surface area. In the burn + 3-AB group, 10 mg/kg of 3-AB was given intraperitoneally 10 min before thermal injury. 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 obtained for biochemical and histopathological analysis. In burn group, the incidence of bacteria isolated from MLN and spleen was significantly higher than other groups (P < 0.05). 3-AB pre-treatment prevented burn induced bacterial translocation and it significantly reduced burn induced intestinal injury. Tissue malondialdehyde and 3-nitrotyrozine levels were found significantly lower than that of the burn group. These data suggest that the relationship between PARS pathway and lipid peroxidation in intestinal tissue and PARS has a role in intestinal injury caused by thermal injury.     

The effects of thermal injury on transcellular permeability and intestinal P-glycoprotein in rats

This study was designed to assess intestinal drug transport via transcellular absorption and intestinal P-glycoprotein content following thermal injury in rats using propranolol as a marker substrate. Male, Sprague Dawley rats (n=30) underwent either a 30% total body surface area full thickness burn or sham treatment. Twenty-four hours later, animals were anesthetized, underwent laparotomy and the proximal jejunum was cannulated. The jejunal segment was perfused with buffer containing [³H] propranolol. Following euthanasia, jejunal tissue was harvested for Western immunoblotting of P-glycoprotein and villin, and immunohistochemical analysis of P-glycoprotein. Dramatic structural changes in jejunal integrity were observed following thermal injury; however, no significant differences in the absorption characteristics of propranolol following thermal injury were observed. Mean effective permeability of propranolol was 5.67±1.79 and 5.85±1.67 cm/s×10⁻⁵ for burn and sham groups, respectively (P>0.05). P-glycoprotein and villin content in the jejunum were significantly decreased in burn animals. The transcellular transport of propranolol is unaffected 24 h following thermal injury in rats, despite alterations in intestinal P-glycoprotein content. The decrease in P-glycoprotein and villin content in thermally injured animals may reflect loss of mature enterocytes at the villus tips.     

Ligustrazine attenuates acute lung injury after burn trauma

Acute lung injury is a common complication in patients with extensive burns in which the burned area exceeds 30% of the total body surface area (TBSA). This study was undertaken to evaluate the effect of Ligustrazine on burn-induced lung injury as well as the release of interleukin-8 (IL-8) in rats to characterize the role of Ligustrazine and IL-8 in lung injury after burn trauma. Sprague-dawley rats were divided into three groups: (1) sham group, rats who underwent sham burn; (2) control group, rats given third-degree burns over 30% TBSA and lactated Ringer solution for resuscitation; and (3) Ligustrazine group, rats given burn injury and lactated Ringer's solution with Ligustrazine inside for resuscitation. Pulmonary injury was assessed at 24 h by pulmonary capillary permeability determined with fluorescein isothiocyanate-labeled albumin and lung histologic analysis, and lung myeloperoxidase (MPO) activity as well as lung wet/dry weight ratio. The IL-8 levels were measured in serum by enzyme-linked immunosorbent assay. These studies showed that burn trauma results in increased pulmonary leakage permeability and lung wet/dry ratio, elevated serum IL-8 levels and MPO activity, and worsened histologic condition. Ligustrazine inhibited these changes, prevented burn-mediated lung injury, and the production of IL-8. This will likely provide further evidence for ligustrazine as a therapeutic strategy in burn-induced lung injury.     

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.     

葛根素对家兔肝缺血再灌注一氧化氮、内皮素-1的影响

目的观察一氧化氮(NO)、内皮素-1(ET-1)在家兔肝缺血再灌注损伤过程中的变化及葛根素(Pur)对其的影响。方法实验家兔随机分为3组:对照组(C组,n=10)、缺血再灌注组(IR组,n=10)和葛根素治疗组(Pur组,n=10)。分别测定缺血前,缺血第45分钟及再灌注第45分钟时肝组织NO,ET-1含量,用电镜观察家兔HIRI及经Pur保护后的肝组织形态学改变。结果家兔缺血再灌注第45分钟时,与C组、Pur组比较:IR组血浆及组织NO含量均明显较低(P<0.01,P<0.05);IR组血浆及组织ET-1含量明显较高(P<0.01,P<0.05);与IR组比较,Pur组肝组织超微结构明显改善。结论葛根素可通过调节机体NO和ET-1水平而对肝缺血再灌注损伤发挥积极的保护作用。     

Sodium butyrate inhibits the production of HMGB1 and attenuates severe burn plus delayed resuscitation-induced intestine injury via the p38 signaling pathway

BackgroundInflammatory response triggered by high mobility group box-1 (HMGB1) protein and oxidative stress play critical roles in the intestinal injury after severe burn. Sodium butyrate, a histone deacetylase inhibitor, has potential anti-inflammatory properties, inhibiting the expression of inflammatory mediators such as HMGB1 in diverse diseases. This study was designed to investigate the effects of sodium butyrate on severe burn plus delayed resuscitation-induced intestine injury, intestinal expressions of HMGB1 and intracellular adhesion molecule-1 (ICAM-1), oxidative stress, and signal transduction pathway changes in rats.Materials and methodsFifty-six Sprague-Dawley rats were divided into 3 groups randomly: (1) sham group, animals underwent sham burn; (2) burn group, rats subjected to full-thickness burns of 30% total body surface area (TBSA) and received 2 ml/kg/TBSA lactated Ringer solution for resuscitation at 6, 12, and 36 h after burn injury; (3) burn plus sodium butyrate (burn + SB) group, animals received burn injury and lactated Ringer solution with sodium butyrate inside for resuscitation in the same manner. Diamine oxidase (DAO) concentration in plasma was measured by enzyme-linked immunosorbent assay. Intestinal fatty acid binding protein (I-FABP) and ICAM-1 expressions in the intestine were analyzed by immunohistochemical method. HMGB1 and p38 mitogen-activated protein kinase (MAPK) expressions in the intestine tissues were examined by Western blot. The intestinal concentration of malondialdehyde (MDA) was also determined.ResultsIntestinal HMGB1 expression was significantly increased in burn group compared with sham group. Sodium butyrate administration significantly inhibited the HMGB1 expression in the intestine, decreased the DAO concentration in plasma, reduced the intestinal I-FABP expression, and improved the intestinal histologic changes induced by burn injury plus delayed resuscitation. Sodium butyrate treatment also markedly reduced the increase of intestinal ICAM-1 expression and MDA content, and inhibited p38 MAPK activity in the intestine of severely burned rats with delayed resuscitation.ConclusionsSodium butyrate inhibits HMGB1 expression which could be attributed to p38 MAPK signal transduction pathway and decreases intestinal inflammatory responses and oxidative stress, thus attenuates burn plus delayed resuscitation-induced intestine injury.     

The delays in intestinal motility and neutrophil infiltration following burn injury in rats involve endogenous endothelins

This study was carried out to investigate the role of endogenous endothelins in intestinal motility following bum injury by using a nonselective endothelin-1 (ET-1) antagonist and to evaluate the ET-1-mediated reactive oxygen metabolite formation and neutrophil infiltration following burn injury. In 2 h and 3 day postburn groups, transit indices were significantly decreased as compared to corresponding sham groups. Transit index was not significantly changed by PD156252 pretreatment in the 2 h postburn group, whereas the delay in transit was abolished in the ET-antagonist treated 3 day postbum group. In the 2 h postburn group, tissue-associated myeloperoxidase (MPO) activity value was found to be increased compared to corresponding sham group, while PD156252 pretreatment partially reversed this effect. Although MPO activity levels were not significantly different between 3 day postburn and corresponding sham groups, MPO levels showed a significant increase in ET antagonist-treated group as compared to the corresponding burn group. In the early phase of the burn, there was no significant difference in protein oxidation levels among the groups. In the 3 day postburn group, protein oxidation levels in ET-antagonist-treated group showed an increase compared to its corresponding burn group. In conclusion, the results demonstrate that endogenous endothelins have an important role in the systemic response to burn injury, as observed by a delay in intestinal motility and an infiltration of neutrophils. Although the results of the animal studies are not readily applicable to burned patients, the present study may suggest that the burned patient's condition should be carefully evaluated to secure a proper and early enteral feeding.     

内皮素及NO在严重烧伤早期胃肠粘膜缺血中的应用

OBJECTIVE: Inadequate perfusion in splanchnic organs and especially in the gut during acute burn period has been reported in many conventionally "successfully" resuscitated patients, but the mechanisms still remain unclear and its early preventive measures need to be further studied. The aim of this study is to evaluate the role of endothelin and nitric oxide in gut ischemia. METHODS: Eighteen male pigs were randomly assigned to one of the three groups: group C, a sham burn group that was subjected to all surgical procedures except burn; group B, sustained 30% TBSA cutaneous thermal burn; Group N, NO donor (C87-3754) was given intravenously (0.0125 mg.kg-1.min-1) at the beginning of resuscitation. RESULTS: In group B, PVF decreased rapidly after burn, and did not recover in the observation period (72 h), ET levels in portal blood and intestinal tissue elevated contrary to the changes in NO. In group N, PVF was higher than in group B. CONCLUSION: 1. Changes in ET and NO may influence the protal blood flow. 2. NO donor was proved to be beneficial in improving GI tissue perfusion by releasing NO.     

Current treatment of severely burned patients.

OBJECTIVE: The authors provide an update on a multidisciplinary approach to the treatment of severely burned patients. A review of studies and clinical trials from the past to the present include fluid resuscitation, sepsis, immune function, hypermetabolism, early excision, wound healing, scar formation, and inhalation injury. SUMMARY BACKGROUND DATA: Advances in treating initial burn shock, infection control, early wound closure, and modulation of the hypermetabolic response have decreased morbidity and mortality in the last two decades. Specialized burn care centers, using a multidisciplinary approach, not only successfully treat large burns and their complications, but provide the necessary rehabilitation and psychological support required for readjustment back into society. CONCLUSIONS: Thermal injury results in a number of physiologic alterations that can be minimized by adequate fluid resuscitation to maintain tissue perfusion, early excision of burn wounds, and rapid wound coverage. These measures, in combination with antibiotic coverage and nutritional support in the form of early enteral tube feedings, will decrease the hypermetabolic response and the incidence of sepsis that can lead to hemodynamic instability and organ failure. Ongoing clinical trials using anabolic agents (e.g., recombinant human growth hormone) and pharmacologic agents that modulate inflammatory and endocrine mediators (e.g., ibuprofen and propranolol) show promise in the treatment of severe burn injuries.     

烧伤延迟复苏与细胞集落刺激因子

为探讨严重烧伤延迟复苏血清粒细胞集落刺激因子（Ｇ－ＣＳＦ）的变化规律及其与感染发生，发展，预后的关系，采用大鼠３０％ＴＢＳＡⅢ度烧伤模型，动态了观察了大鼠在立即复苏与延迟复苏两种条件下，外周血白细胞数量，血清（Ｇ－ＣＳＦ）和肿瘤坏死因子－α（ＴＮＦ－α）含量，中性粒细胞吞噬功能；采用大鼠３０％ＴＢＳＡⅡ度烧伤延迟复苏合并早期创面感染模型，动态观察应用重组粒细胞－巨噬细胞集落刺激因子（ｒｈＧＭ－ＣＳ     

Septicaemia after burn injury: a comparative study

Seventy-nine (8.4%) patients during June 1992–May 1996 (Group-1) and 68 (7.2%) patients from June 1996 to May 2000 (Group-2) who developed septicaemia at the burns unit of Al-Babtain Centre for Plastic Surgery and Burns, Kuwait, were retrospectively studied and compared. The mean age of 26 years, male predominance, flame burns as main aetiology and mean burn percentage of ≥40% was observed in both the groups. Both groups revealed extensive flame burn, inhalation injury, intubation and difficult resuscitation as the risk factors. The proportion of satisfactory resuscitation increased significantly (P<0.001) in Group-2. The septicaemia commonly occurred within 2 weeks postburn but the number of episodes during 5 days postburn was less in Group-2. The surface wound was found to be the likely source of entry of the organisms into the blood stream in both the groups. The gram positive organisms were dominant aetiologic factor in both groups but an increase frequency of Acnetobacter was found in Group-2. The proportion of MRSE and Pseudomonas septicaemia was significantly higher (P<0.01) in the Group-1. The rate of survivors, in both the groups was higher among operated patients but it was significantly higher (P<0.001) in the Group-1. A mortality rate 20.6% in Group-2 decreased against Group-1, which can be attributed to better resuscitation, nutritional care, early detection of septicaemia, appropriate antibiotics and early wound excision and skin grafting. MOF was the cause of death of 60.9% in Group-1 and 85.7% in Group-2. There was no role of prophylactic antibiotic in burn patients in the incidence of septicaemia and mortality.     

大鼠烧伤早期肝功能及超微结构改变和药物保护作用的观察

为探讨烧伤及液体复苏后肝损害以及药物的保护作用，采用大鼠３０％ＴＢＳＡⅢ度烫伤模型，将１２６只Ｗｉｓｔａｒ大鼠随机分为正常对照组、早期复苏组、早期复苏＋药物治疗组、延迟复苏组、延迟复苏＋药物治疗组及不治疗组。观察烧伤后６，１２，２４及４８小时血清ＡＬＴ、ＡＳＴ含量变化，同时对肝细胞光镜及电镜下组织病理学改变进行了观察。结果表明：早期复苏及延迟复苏组血清ＡＬＴ、ＡＳＴ及肝细胞形态均出现异常，ＡＬＴ在伤后６小时即显著升高，２４小时达到峰值水平，ＡＳＴ变化与ＡＬＴ相似。病理检查显示肝细胞有不同程度损害。给予爱维治药物治疗后，上述损害均得到改善。结果提示：肝脏是烧伤早期易受损伤的器官之一，延迟复苏将进一步加重肝组织损伤；爱维治有益于保护肝细胞结构和功能。     

前列腺素E1在酸吸入性急性呼吸窘迫综合征中的肺保护作用

目的 研究静脉注射前列腺素E1（PGE1）能否阻止酸吸入性急性呼吸窘迫综合征（ARDS）的发生。方法 20只新西兰兔在稀HCI经右支气管滴入后随机分成两组：（1）损伤组（n＝10）在酸滴入后维持机械通气，未行其它治疗；（2）治疗组（n＝10）在酸滴入后即刻缓慢静注PGE1并维持。在基础状态及酸滴入后记录血气、气道压力并抽动脉血测定6－K－PGF1α、TXB2、NO^-2／NO^-3和ET－1，动物处死后测定右肺的湿干比（W／D）值及测定右肺支气管肺泡灌洗液（BALF）中总蛋白（TP）的水平，并作肺组织形态学观察。结果 治疗组在酸滴入后血氧分压（PaO2）显著高于损伤组。治疗组血浆6－K－PGF1α和NO^-2/NO^-3水平显著高于损伤组，而血浆TXB2和ET－1水平显著低于损伤组，治疗组右肺W／D和TP显著低于损伤组。损伤组右肺呈弥漫性损伤，而治疗则见损伤呈局灶治疗组右肺W／D和TP显著低于损伤组。损伤右肺呈弥漫性炎性损伤，而治疗组则见损伤呈局灶性，且其病理损伤程度较损伤组明显减轻。结论 （1）酸吸入后即刻应用PGE1可减轻ARDS的范围和严重程度；（2）PGE1保护了肺血管内皮细胞，使内源性PGI2／TXA2和NO／ET－1的产生保持平衡，有利地减轻ARDS。     

An analysis of death in older burn patients

Between August 1976 and July 1986, 110 burn patients over the age of sixty-five were admitted to the Burn Unit of Ruijin Hospital. The average extent of burn was 19.9% TBSA (0.5-90%), with 14.7% full thickness (0.5-90%). There was a significant difference surface and full thickness area (P less than 0.001) of total burn between non-survival and survival patients. The analysis of causes of death in elderly burn patients suggested that the preexisting cardiopulmonary diseases and inhalation injury appeared particularly important since pneumonia was considered as a primary cause of death in 13 patients, myocardial infarction in 2, congestive heart failure in 2. The resuscitation, early excision of deep burn wound and grafting, prevention and treatment of other complications, and nutritional supplement can decrease the mortality of elderly burn patients.     

大鼠烧伤早期肝功能及超微结构改变和药物保护作用的观察

为探讨烧伤及液体复苏后肝损害以及药物的保护作用,采用大鼠30%TBSAⅢ度烫伤模型,将126只 Wistar 大鼠随机分为正常对照组、早期复苏组、早期复苏 药物治疗组、延迟复苏组、延迟复苏 药物治疗组及不治疗组。观察烧伤后6,12,24及48小时血清 ALT、AST 含量变化,同时对肝细胞光镜及电镜下组织病理学改变进行了观察。结果表明:早期复苏及延迟复苏组血清 ALT、AST 及肝细胞形态均出现异常,ALT 在伤后6小时即显著升高,24小时达到峰值水平,AST 变化与 ALT 相似。病理检查显示肝细胞有不同程度损害。给予爱维治药物治疗后,上述损害均得到改善。结果提示:肝脏是烧伤早期易受损伤的器官之一,延迟复苏将进一步加重肝组织损伤;爱维治有益于保护肝细胞结构和功能。