Role of nitric oxide in Toll-like receptor 2 and 4 mRNA expression in liver of acute hemorrhagic necrotizing pancreatitis rats

AIM： To investigate the role of nitric oxide （NO） in Tolllike receptor 2 （TLR2）/4mRNA expression in livers of acute hemorrhagic necrotizing pancreatitis （AHNP） rats. METHODS： One hundred and ten SD male rats were randomly divided into sham-operated group （n = 10）, AHNP group （n = 30）, chloroquine （CQ）-treated group （n = 30） and L-Arg-treated group （n = 40）. TLR2/4mRNA expression in the liver of AHNP rats was measured by RT-PCR. RESULTS： Expression of TLR2/4mRNA could be detected in the liver of AHNP rats in sham-operated group （0.155E-5±0.230E-6 and 0.115E-2±0.545E-4）, but was markedly increased at 3 h in AHNP group （0.197E-2±0.114E-3 and 0.175±0.349E-2） peaking at 12 h （0.294E-2 ± 0.998E-4 and 2.673 ± 2.795E-2, P〈 0.01）. Hepatic injuries were aggravated, TNF-α concentration in the liver was increased and NO concentration was decreased （P〈 0.05 or P〈 0.01）. When TLR2/4mRNA expression was inhibited by CQ （3 h： 1.037E-4±3.299E-6 and 0.026±3.462E-3; 6 h： 1.884E-4±4.679E-6 and 0.108±6.115E-3; 12 h： 2.443E-4±7.714E-6 and 0.348±6.807E-3; P 〈 0.01）, hepatic injuries were relieved, NO concentration in the liver was increased and TNF-α concentration was decreased （P〈0.05 or P〈0.01）. When rats with AHNP were treated with L-Arg, TLR2/4mRNA expression in the liver could be effectively inhibited （50 mg-T： 0.232E-2±0.532E-4 and 0.230±6.883E-3; 100 mg-T： 0.210E-2± 1.691E-4 and 0.187±0.849E-2; 200 mg-T： 0.163E-2±0.404E-4 and 0.107±0.195E-2; 400 mg-T： 0.100E-2±0.317E-4 and 0.084±0.552E-2; P〈0.01） and hepatic injuries were relieved. At the same time, NO concentration in the liver was markedly increased and TNF-α concentration was decreased （P〈0.05 or P〈O.OI）, CONCLUSION： The expression of TLR2/4mRNA is increased and hepatic injuries are aggravated in the liver of AHNP rats. TLR2/4mRNA gene expression in the liver of AHNP rats can be markedly inhibited by NO, leading to the relief of hepatic injuries.

EFFECT OF SOMATOSTATIN ON THE EXPRESSION OF TNF α mRNA IN MULTIORGANS OF RATS WITH ACUTE HEMORRHAGIC NECROTIC PANCREATITIS

Objectives.To study the expression of TNF α mRNA and the effect of somatostatin on the expression of TNF α mRNA in multiorgans of rats with acute hemorrhagic necrotic pancreatitis(AHNP). Methods.AHNP in the rat was induced by retrograde injection of 5% sodium taurocholate into the bile-pancreatic duct. Somatostatin octapeptide (SS-OP) (2μg/kg)was injected into the femoral vein imme- diately in rats of the treatment group after inductive AHNP. Rats of the sham operative group received in- jection of saline. Sixty animals of the AHNP and sham operative groups at the designated time(0. 2h, 0. 5 h, 2h, 4h, 8h, after the operation,six animals at each time point)and tweleve animals of treatment group at 4h after the operation were sacrificed for samples of pancreas, liver and lung. The expressions of TNF α mRNA within the pancreas, liver and lung were established by RT－PCR. Results. TNF α mRNA became detectable in the pancreas as early as 0. 2h after inductive AHNP, while it was undetectable in other organs until 0. 5h. Expression of TNF α mRNA in each tissue increased continuously and reached a peak at 4h,demonstrating a significant difference compared with that at 0. 5h and 8h. Expressions of TNF α mRNA from pancreas, liver and lung were decreased 50-80% in the treat- ment group, the pancreatic necrosis was also attenuated dramatically. Conclusion. TNF α mRNA was detectable in pancreas,liver and lung tissues at the early stage of AH- NP.SS-OP can significantly inhibit the expression of TNF α mRNA and attenuate the pancreatic necrosis. We feel that this may be an important mechanism of SS-OP in the treatment of AHNP.

Effect of nitric oxide on toll-like receptor 2 and 4 gene expression in rats with acute lung injury complicated by acute hemorrhage necrotizing pancreatitis

BACKGROUND: Toll-like receptor (TLR) 2/4 might play important roles in mediating proinflammatory cytokine synthesis and release. And nitric oxide (NO) has been used to treat acute respiratory distress syndrome (ARDS). This study aimed to investigate the changes in TLR2/4 gene expression in the lungs of rats with acute lung injury (ALI) complicated by acute hemorrhage necrotizing pancreatitis (AHNP) and the effect of NO on the TLR2/4 gene expression. METHODS: One hundred and ten SD male rats were randomly divided into sham-operated group ( n = 10) , AHNP group (n = 30) , chloroquine-treated group ( n = 30) , and L-Arg-treated group (n =40). The lungs were dissected for lung histological scoring, and bronchoalveolar lavages were harvested for lung injury indexing. TLR2/4 mRNA expression in the lungs was measured by RT-PCR. RESULTS: TLR2/4mRNA was detected in the lungs with low values in the sham-operated group (0.016±0. 210E-2, 0.112 ±0.750E-2) , but it was markedly increased at 3 hours in the AHNP group (0.787±0.751E-2, 1.512 ±1.794E-2) , peaking at 12 hours (1.113 ±6.141E-2, 2.957±2.620E-2; P <0.05 or P <0.01). When lung injuries were aggravated, TNF-α concentrations in the lungs were increased, but NO concentrations were decreased ( P < 0.05 or P < 0.01 ) . When TLR2/4mRNA was inhibited by CQ (3h: 0.313 ± 5.491E-2, 0.005 ±1.419E-3 ; 6h: 0.488 ±7.442E-2, 0.010 ± 1.518E-3; 12h: 0.883 ± 8.911E-2, 0.024 ± 2.760E-3; P< 0.05 or P <0.01) , lung injuries were relieved. NO concentrations in the lungs were increased but TNF-α concentrations were decreased (P <0. 05 or P <0.01). When the rats with AHNP were treated with L-Arg, TLR2/4mRNA expression in the lungs could be effectively inhibited (50mg-T: 0.656 ±3. 977E-2, 1. 501 ±6.111E-2; 100mg-T: 0.260± 0.891E-2, 0.732 ±5.135E-2; 200mg-T: 0.126 ±0.914E-2, 0.414 ± 1.678E-2; 400mg-T: 0.091 ±0.399E-2, 0.287 ± 0.176E-2; P <0.05 or P <0. 01) and lung injuries were relieved. At the same time, NO concentrations in the lungs were markedly increased, but TNF-α concentrations were decreased (P <0.05 or P <0.01). CONCLUSIONS: The expression of TLR2/4mRNA is increased in the lungs in rats with AHNP and lung injuries are aggravated. TLR2/4mRNA gene expression of the lungs of rats with AHNP could be markedly inhibited by NO, leading to the relief of lung injuries.

Chloroquine Relieves Acute Lung Injury in Rats with Acute Hemorrhagic Necrotizing Pancreatitis

Summary： This study preliminarily investigated the mechanism by which chloroquine （CQ） relieves acute lung injury （ALI） complicated in acute hemorrhagic necrotizing pancreatitis （AHNP）. Sixty male Wistar rats were randomized into sham-operated group （group A, n=10）, AHNP group （group B, n=10）, L-arginine-treated group （group C, n=10）, L-N-nitro-L-arginine methyl ester （NAME）-treated group （group D, n=10）, CQ-treated group （group E, n=10） and CQ＋L-NAME-treated group （group F, n=10）. TLR4 expression was measured by using real time-PCR and Western blotting respectively. The results showed that, in the group B, the expression of TLR4 and the levels of TNF-α and IL-6 in the lungs were significantly increased, and the nitric oxide （NO） concentration was reduced, as compared with those in the group A （P〈0.05 or P〈0.01）. Lung injury was aggravated with the increased expression of TLR4. When the inhibitor and stimulator of TLR4, namely L-Arg and L-NAME, were added respectively, lung injury was correspondingly relieved or aggravated （P〈0.05 or P〈0.01）. In the group E, TLR4 expres- sion was substantially lower and NO concentration higher than those in the group B （P〈0.05 or P〈0.01）. However, in the group F, NO concentration was markedly decreased, and the inhibitory effect of CQ on TLR4 expression and the relief of lung injury were weakened when compared with those in the group E （P〈0.05 or P〈0.01）. It was concluded that TLR4 may play an important role in the pathogenesis and development of ALl complicated in AHNP. CQ could relieve ALl by decreasing the TLR4 expression and increasing the NO release.

ANALYSIS OF DEATH FACTORS FOR ACUTE HEMORRHAGIC NECROTIZING PANCREATITIS

Objective:To analyse the factors affecting the mortality of acute hemorrhagic necrotizing pancreatitis (AHNP). Methods:One hundred and twelve patients with AHNP were retrospectively divided into two groups——the dead and survivors. Some parameters were analysed statistically.Results:The average age,sex ratio and onset of illness were similar between two groups. The difference of early shock, early ARDS, high body temperature, leukocytosis and high blood glucose between two groups were not significant. The important factors affecting the mortality were: severe pancreatic necrosis; incorrect therapeutic surgery;improper surgical methods.Conclusion: The patients with mild or moderate AHNP should mainly receive conservative treatment for 48～72 hours. The early shock and ARDS should be corrected before surgical intervention, the swelling pancreas should be dissected fully and duodenostomy should be performed in operation.

Clinical Significance of Serum Myelin Basic Protein in Patients with Severe Acute Pancreatitis

Objective In order to determine serum myelin basic protein (MBP) in patients with severe acute pancreatitis and evaluate its clinical significance. Methods\ Serum MBP was measured in 20 patients with acute hemorrhagic necrotic pancreatitis (AHNP) and in 20 normal subjects by enzyme linked immunoabsorbent assay. Results\ Serum MBP content of AHNP group was significantly higher than that of normal control group (P<0.05). Serum MBP content in patients with pancreatic encephalopathy (PE) was significantly higher than that of those without PE (P<0.05). Conclusion\ ①Serum MBP content in patients with AHNP increased significantly;②Serum MBP content may reflect brain injury and its severity;③The prognosis of AHNP is correlated with its serum MBP content.\;

青葙子苷A对AHNP诱导肝损伤的保护作用研究

为研究青葙子苷A对大鼠急性出血性坏死性胰腺炎(AHNP)诱导肝损伤的治疗作用及其初步作用机制,应用逆行胰胆管术注射牛磺胆酸钠(TAC)复制了AHNP试验动物模型,将其分为假手术组(A组)、AHNP生理盐水对照组(B组)、AHNP青葙子苷A高、低剂量治疗组(C、D组)和AHNP奥曲肽治疗组(阳性药物对照,E组)。各组试验动物手术后6 h处死,测定腹水量,运用比色法检测其血清淀粉酶含量,ELISA法测定肝组织中TNF-α含量,HE染色观察其肝组织病理变化,透射电镜观察肝脏卵圆细胞形态变化,Western-Blot检测肝组织中细胞核转录因子(NF-кB)蛋白的表达情况。结果表明,与A组比较,AHNP生理盐水对照组(B组)大鼠肝组织中腹水量、血清淀粉酶含量、TNF-α含量明显升高,NF-кB蛋白表达明显增强;青葙子苷A治疗组(C、D组)和奥曲肽治疗组(E组)肝组织中腹水量、血清淀粉酶含量、TNF-α含量及NF-кB蛋白表达均较B组显著(P<0.05)降低。说明青葙子苷A对AHNP诱导的肝损伤有显著的保护作用,其机制可能是通过抑制胰弹性蛋白酶的分泌与激活,抑制NF-кB表达,降低炎症反应,从而减轻肝损伤。

黄芪注射液通过调控mTOR/p70S6K信号通路对急性出血坏死型胰腺炎肺损伤炎症反应的影响

背景急性出血坏死型胰腺炎是临床常见的消化系统急症,肺损伤是其常见并发症和致死原因.黄芪注射液具有调节内分泌、增强免疫力、抑制病毒、抗炎、抗氧化应激等作用,但目前尚未见关于黄芪注射液在重症急性胰腺炎肺损伤中的相关研究.目的分析黄芪注射液通过调控雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)/核糖体70S小亚基S6蛋白激酶(ribosome 70S small subunit S6 protein kinase,p70S6K)信号通路对急性出血坏死型胰腺炎(acute hemorrhagic necrotic pancreatitis,AHNP)肺损伤炎症反应的影响.方法48只成年SD大鼠简单随机化分为对照组、模型组、低、中、高黄芪注射液组、阳性对照组,各8只,记录各组胰腺与肺组织组织病理学变化,比较各组Schmidt评分、血清淀粉酶(amylase,AMS)Hofouaer评分、动脉血二氧化碳分压(PaCO_(2))、动脉血氧分压(PaO_(2))、炎症因子[肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)、白介素-6(interleukin-6,IL-6)]、mTOR/p70S6K信号通路蛋白[mTOR、p70S6K、p-p70S6K、p-mTOR、真核启动因子4E结合蛋白1(p-4E binding protein 1,4EBP1)]水平.结果对照组胰腺、肺组织无异常变化;模型组胰腺实质呈片状坏死、充血水肿,胰腺腺泡细胞与间质细胞大量破坏,小叶结构紊乱,大量炎症细胞浸润与红细胞溢出,肺泡结构排卵紊乱、间质水肿、炎性细胞浸润、肺泡间隔增宽、灶性或片状肺不张、出血;低、中、高黄芪注射液组胰腺与模型组相比,呈现出不同程度改善,且随黄芪注射液剂量增加,改善程度依次增加,其中高黄芪注射液组与阳性对照组组织病理呈现出相似特征;模型组Schmidt评分、AMS、Hofouaer评分PaCO_(2)均高于对照组,PaO_(2)均低于对照组(P<0.05);低、中、高黄芪注射液组Schmidt评分、AMS、Hofouaer评分PaCO_(2)依次降低,PaO_(2)依次升高(P<0.05);模型组TNF-α、IL-6高于对照组(P<0.05);低、中、高黄芪注射液组TNF-α、IL-6依次降低(P<0.05);模型组mTOR、p70S6K、p-p70S6K、p-mTOR、4EBP1高于对照组(P<0.05);低、中、高黄芪注射液组mTOR、p70S6K、p-p70S6K、p-mTOR、4EBP1依次降低(P<0.05).结论黄芪注射液可呈剂量依赖性改善AHNP血气指标、炎症反应、胰腺与肺组织病理状态,其机制可能是通过调控mTOR/p70S6K信号通路实现的,抑制mTOR/p70S6K信号通路可能为AHNP肺损伤的治疗提供了一个新思路.

CT影像学分级用于急性坏死性胰腺炎病情判别及预后评估的意义

目的：研究急性出血性坏死性胰腺炎的ＣＴ分类标准和预后的意义。材料与方法：搜集急性坏死性胰腺炎３９例，早期均行非手术治疗，均于入院后７２小时内行动态ＣＴ扫描，按ＣＴ影像学表现，将胰腺坏死分为３型，即点片状坏死、段状坏死（坏死部分超过整个胰腺的１／３，坏死范围贯穿胰腺全层）、全胰腺坏死（超过胰腺８０％的段状坏死）。点片状坏死作为基本记分，坏死部位分为胰头、胰体及胰尾，每一部位计１分；段状坏死３分；全胰腺坏死计６分。渗出部位按左右肾前筋膜、小网膜囊、胰腺被膜下及腹水统计，每一部位计１分。按ＣＴ影像学的表现进行分级，总分≤３分为轻型，４～５分为中型，≥６分为重型。临床病情严重程度及预后的判别指标：发热时间（体温超过３８℃）、禁食时间、住院时间、器官功能受损情况、假性囊肿形成情况、中转手术率及死亡率等。按ＣＴ影像学分级的不同类型的患者进行统计分析，３９例患者又按Ｂａｌｔｈａｚａｒ分级。结果：Ｅ级２０例，Ｄ级１２例，Ｃ级７例，各级与临床病情轻重及预后无相关性。按本方法进行ＣＴ分级，３９例患者中，轻型１２例，中型１７例，重型１０例。轻型患者的临床恢复过程较重型顺利，轻型及中型患者的中转手术率及死亡率均较重型患者明显为低。?

急性胰腺炎病因的病理学探讨

胰胆管内逆行注射 5 .0 %牛磺胆酸钠溶液 ,建立大鼠急性出血坏死性胰腺炎 (AHNP)模型 ,通过光镜普通染色、PTH染色及电镜超微结构方法 ,对诱导AHNP后 5min至 6h胰腺的病变及微循环的形态学表现进行观察 ,以探讨胰腺炎的病因和发病机制。发现 :诱导AHNP后主要病变为 :胰腺组织出血、坏死 ,白色血栓、微血栓及混合血栓形成 ;并且随着诱导时间的延长病变加重。提示

血液流变学异常在急性出血坏死性胰腺炎发病机理中的意义

作者制成犬急性出血坏死性胰腺炎(AHNP)模型,并对其血液流变学变化进行了系统观察。发现在犬AHNP早期,其血液流变学即发生显著异常,并随病程进展而加重,导致胰腺微循环障碍,使胰腺炎病变不断恶化;使用药物改善血液流变学异常后,胰腺炎病变即有明显好转。表明血液流变学异常在AHNP病变恶化过程中占有重要地位。并提示改善血液流变学的药物对AHNP的治疗是有益的。

一氧化氮对急性出血坏死性胰腺炎肝脏中Toll样受体2/4 mRNA表达的影响

目的探讨一氧化氮(NO)对于急性出血坏死性胰腺炎(AHNP)时肝脏中T o ll样受体2/4(TLR 2/4)mRNA表达的影响。方法采用牛磺胆酸钠(TAC)逆行胰胆管注射制备AHNP肺损伤大鼠模型。动物分为假手术组、胰腺炎组和L精氨酸(L A rg)治疗组。假手术组于术后6 h,胰腺炎组和L A rg组分别于术后3、6、12 h取静脉血和肝组织,测定血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(A ST)、淀粉酶和肝组织NO,逆转录聚合酶链反应(RT PCR)方法检测不同时间点肝组织肿瘤坏死因子α(TNFα)、TLR 2/4mRNA表达变化。结果与假手术组比较,胰腺炎组大鼠3 h肝组织TLR 2/4 mRNA表达开始增高〔(1.970±0.362)×10-3,(175.000±0.111)×1-0 3比(1.150±0.725)×10-6,(11.450±1.724)×10-4,〕12 h表达达峰值〔(2.940±0.316)×1-0 3,(2 673.000±88.380)×1-0 3,P均<0.01〕;血清淀粉酶ALT、A ST 3 h后即升高,肝损伤加重,肝组织TNFαmRNA表达升高,NO浓度逐渐降低(P<0.05或P<0.01);给予L A rg治疗后,NO浓度升高(P<0.05),TLR 2/4 mRNA表达降低〔3 h:(0.351±0.153)×1-0 3,(135.000±22.310)×1-0 3;6 h:(2.100±0.535)×10-3,(187.000±26.850)×1-0 3;12 h:(2.620±0.208)×1-0 3,(1 959.000±270.000)×10-3;P<0.05或P<0.01〕,血清淀粉酶、ALT、A ST均降低,肝损伤减轻,肝组织TNFαmRNA降低(P<0.05或P<0.01)。结论AHNP时,肝组织内TLR 2/4 mRNA表达上调,肝组织损伤加重;NO可以明显抑制AHNP肝组织TLR 2/4 mRNA的表达。

早期应用L-精氨酸治疗急性出血坏死性胰腺炎的实验研究

目的 :探讨早期应用L 精氨酸对急性出血坏死性胰腺炎 (AHNP)的治疗作用。方法 :经大鼠胰胆管注射牛磺酸钠制备AHNP模型 ,分别静注L 精氨酸、生理盐水、山莨菪碱 ;观察血清淀粉酶、白介素 6 (IL 6 )、丙二醛 (MDA)、一氧化氮 (NO)改变及胰腺的病理改变。结果 :应用L 精氨酸后 ,能升高血NO浓度 ,清除氧自由基 ,降低血清IL 6水平 ,降低血清淀粉酶 ,改善胰腺病变 ,其作用优于山莨菪碱。结论 :早期应用一定剂量的L

中药腹腔灌洗对急性出血坏死性胰腺炎大鼠肠道细菌移位的影响

目的 :通过腹腔灌洗对制备的大鼠急性出血坏死性胰腺炎 (AHNP)模型治疗 ,观察各种腹腔灌洗液对AHNP时细菌移位的治疗作用。方法 :Wistar大鼠 16 0只 ,随机分成 :对照组、AHNP组、抗生素间断灌洗组、抗生素持续灌洗组、中药间断灌洗组、中药持续灌洗组 ,进行腹腔灌洗 ,并行血液、腹腔渗液细菌培养 ,胰腺病理检查。结果 :AHNP组胰腺病理损害严重 ,血液、腹腔渗液细菌培养阳性率分别为 80 %和 90 %。中药腹腔灌洗组与AHNP组比较 ,上述病理变化明显减轻 ,血液、腹腔渗液细菌培养阳性率均下降至 4 0 %。结论 :AHNP时肠粘膜屏障功能受损 ,发生细菌移位 ,导致肠源性胰腺感染。中药腹腔灌洗对防止细菌移位有一定的作用 ,也可减轻AHNP的病理损害。

抗生素腹腔灌洗治疗急性出血坏死性胰腺炎效果的观察

目的 :探讨白介素 6 (IL 6 )、IL 8和肿瘤坏死因子 α(TNFα)在急性出血坏死性胰腺炎 (AHNP)发病中的作用 ,并观察各种腹腔灌洗液对 AHNP的治疗效果。方法 :将 12 0只大鼠随机分成 :正常对照组、AHNP组、抗生素持续灌洗组和抗生素间断灌洗组。采用 5 %牛磺胆酸钠逆行胆胰管注射建立大鼠 AHNP模型 ,并于模型制成后 2 4、48、72小时取血液、腹水、胰腺组织 ,测定血液、腹水中 IL 6、IL 8、TNFα水平 ,作胰腺病理检查。结果 :AHNP组大鼠各时间点血液、腹水中 IL 6、IL 8、TNFα水平较对照组明显增高 (P均 <0 .0 5 ) ,并随病情加重而升高 ,且胰腺组织学改变进行性加重 ,胰腺病理损害评分明显增高 (P<0 .0 5 )。抗生素腹腔灌洗治疗组各时间点上述指标水平均有所降低 ,胰腺病理损害减轻 ,抗生素持续腹腔灌洗组病理评分分别小于 AHNP组相应时间点 (P均 <0 .0 5 )。结论 :IL 6、IL 8、TNFα参与 AHNP发病机制 ,抗生素腹腔灌洗能够降低血液、腹水中 IL 6、IL 8、TNFα水平 ,减轻胰腺组织的损害。

内源性一氧化氮在急性出血坏死性胰腺炎发病中的作用

为探讨内源性一氧化氮 (NO)在急性出血坏死性胰腺炎 (AHNP)发病中的作用 ,胰胆管内逆行注射 5 %牛磺胆酸钠 ,建立大鼠急性出血坏死性胰腺炎模型 ,通过光镜观察胰腺的病理变化 ,用免疫组化SP法测定胰腺微血管内皮细胞内eNOS的表达 ,用Westernblot分析胰腺组织内iNOS的表达。结果 :诱导AHNP后 5min就出现胰腺微血管的病变 ,并伴有腺泡细胞凝固性坏死。随着时间的延长 ,上述病变加重。术后 1 0min ,胰腺间质小血管内皮细胞表达eNOS开始显著增高 (P <0 .0 5 ) ,并随着疾病的发展而逐渐增高。术后 5min,胰腺组织内iNOS表达开始增高 (P <0 .0 5 ) 。

急性出血坏死性胰腺炎小鼠辅助性T细胞亚群1/2的变化规律及中药干预作用研究

目的:探讨急性出血坏死性胰腺炎小鼠早期出现辅助性T细胞(T h)亚群T h1/T h2变化规律,观察参麦注射液及黄芪注射液的干预作用。方法:65只昆明小鼠随机分为假手术组5只,胰腺炎组、参麦治疗组、黄芪治疗组各20只。采用腹腔连续注射雨蛙素50μg/kg,每次间隔1 h,连续注射6次后,向腹腔内注射脂多糖造成小鼠急性出血坏死性胰腺炎模型。治疗组分别在制模后向腹腔内注射参麦注射液或黄芪注射液,于末次注射完毕后2、6、12和24 h,分别测定各组动物血浆淀粉酶及脾细胞的T h1/T h2比值,观察胰腺及小肠病理变化。结果:胰腺炎组制模后6 h胰腺病理及血浆淀粉酶提示出现急性出血坏死性胰腺炎,同时出现脾细胞T h1/T h2比值失衡(P<0.01),并逐渐加重,在24 h时甚至出现倒置。而中药治疗组此种变化较轻,在制模后24 h参麦注射液较黄芪注射液疗效更显著(P<0.05)。结论:小鼠急性出血坏死性胰腺炎早期出现免疫失衡,参麦注射液和黄芪注射液对此有调节作用。

清胰汤对急性出血坏死性胰腺炎大鼠肠屏障功能障碍的保护作用

目的探讨清胰汤对急性出血坏死性胰腺炎(AHNP)大鼠肠屏障功能障碍(IBD)的保护作用。方法 SD大鼠随机分成AHNP组、AHNP+清胰汤治疗(QYT)组和假手术(SO)组。AHNP组与QYT组大鼠建立AHNP模型,SO组大鼠仅开腹翻动胰腺。QYT组造模后进行清胰汤胃灌注,另两组生理盐水灌胃,24 h后检测门静脉血二胺氧化酶(DAO)、内毒素(ET)浓度,小肠组织病理学评分,小肠黏膜电镜观察。结果 QYT组血DAO及ET浓度、小肠病理组织学评分均低于AHNP组,电镜结果好于AHNP组。结论清胰汤可显著降低实验性AHNP大鼠门静脉血中二胺氧化酶和内毒素浓度,减少肠黏膜损伤,可在一定程度上减轻AHNP大鼠肠屏障功能障碍的严重程度。

川芎嗪对急性出血坏死性胰腺炎大鼠肺损伤的作用及机制研究

急性出血坏死性胰腺炎大鼠随着时间延长,肺部郁血加重,肺系数增加;肺间质中性粒细胞浸润增多,肺间质及肺泡水肿、肺不张;电镜改变为Ⅱ型上皮细胞板层小体减少,线粒体、内质网肿胀,随着肺损伤程度加深,血浆TXB_2/6-keto-PGF_(1α)比值及LPO值增加。川芎嗪显著降低了TXB_2/6-keto-PGF_(1α)比值,降低LPO值;降低肺系数,肺组织病理形态改善,大鼠存活率提高。

急性出血坏死性胰腺炎术后早期实施肠内营养的临床研讨

探讨急性出血坏死性胰腺炎（ ＡＨＮＰ） 患者术后早期经空肠造瘘管实施肠内营养（ ＥＮ） 的安全性、可行性及有效性。本组３８ 例患者分为术后３ ～４ 天开始ＥＮ 的早期组和术后７ 天开始ＥＮ 的后期组，均经空肠造瘘管持续滴注肠内营养液，并由肠外营养逐步过度到ＥＮ。测定２ 组患者的耐受性指标（ 血淀粉酶、血糖及肝功能） 、有效指标（ 血浆白蛋白）并观察临床症状： 有无腹痛及腹部体征。结果： 耐受性指标２ 组均在正常范围，而有效性指标提示早期组的血浆白蛋白值升高较快、低蛋白血症的纠正比后期组早，２ 组均无腹痛等现象。提示ＡＨＮＰ 患者术后早期实施ＥＮ 是安全、可行和有效的，它能提高治愈率，在治疗ＡＨＮＰ 中起到重要的作用。