Effects of Enalaprilat on Acute Necrotizing Pancreatitis in Rats

The aim of this study was to investigate the influence of enalaprilat on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats. The induction of ANP resulted in a significant increase in the mortality rate, pancreatic necrosis, serum activity of amylase, alanine aminotransferase (ALT), and interleukin-6 (IL-6), lactate dehydrogenase (LDH) in bronchoalveolar lavage (BAL) fluid, serum concentration of urea, and tissue activity of myeloperoxidase (MPO) and maondialdehyde (MDA) in the pancreas and lung, and a significant decrease in concentrations of calcium, blood pressure, urine output and p0₂. The use of enalaprilat inhibited the changes in urine output, blood pressure, serum concentration of urea, p0₂, and tissue activity of MPO and MDA in the pancreas and lungs. It reduced the mortality and pancreatic damage. Enalaprilat demonstrated a beneficial effect on the course of ANP in rats; therefore, it may be used in the treatment of acute pancreatitis. Part of this study was presented at the 40th Congress of the European Surgical Research Society on 25–29 May 2006, in Rostock, Germany.     

Effects of the Celecoxib on the Acute Necrotizing Pancreatitis in Rats

The investigation of the effects of the celecoxib as a cylooxygenase-2 (COX-2) inhibitor on the course of the acute necrotising pancreatitis (ANP) in rats. ANP was induced in 72 rats by standardized intraductal glycodeoxycholic acid infusion and intravenous cerulein infusion. The rats were divided into four groups (six rats in each group): Sham + saline, sham + celecoxib, ANP + saline, ANP + celecoxib. Six hours later after the ANP induction, celecoxib (10 mg/kg) or saline was given i.p. In the 12th hour, routine cardiorespiratuar, renal parameters were monitored to assess the organ function. The serum amylase, alanine amino transferase (ALT), interleukin 6 (IL-6), lactate dehydrogenase (LDH) in bronchoalveolar lavage (BAL) fluid, the serum concentration of the urea, the tissue activity of myeloperoxidase (MPO) and malondialdehyde (MDA) in pancreas and lungs were measured. The pancreas histology was examined. In the second part of the study, 48 rats were studied in four groups similar to the first part. Survival of all the rats after the induction of ANP was observed for 24 h. The induction of the pancreatitis increased the mortality from 0/12, in the sham groups to 4/12 (30%) in the acute pancreatitis with saline group, 5/12 (42%) in the acute pancreatitis with celecoxib group respectively, heart rate, the serum activities of amylase, ALT, the tissue activities of MPO, MDA in the pancreas and lung, and LDH in BAL fluid, the serum concentration of the urea and IL-6, the degree of the pancreatic damage and decreased the blood pressure, the urine production, pO₂ and the serum concentration of calcium. The use of celecoxib did not alter these changes except the serum IL-6 concentration, urine production and MPO, MDA activities in the tissue of the lungs and pancreas. Serum urea concentration and pancreatic damage in ANP + celecoxib group were insignificantly lesser than ANP + saline group. Whereas treatment with celecoxib improves lung and renal functions, the degree of pancreatic damage partially and the serum IL-6 level completely, it does not improve the cardiovascular and liver functions, the mortality rate and the calcium level. Celecoxib may be useful for the support of some organ functions during ANP in rats.     

急性坏死性胰腺炎大鼠垂体功能和结构的变化

目的:观察大鼠垂体组织结构及功能在急性坏死性胰腺炎(ANP)时的变化情况。方法:雄性SD大鼠72只,随机分为正常对照组(N组),假手术(SO)1h、3h、6h、12h组,ANP1h、3h、6h、12h组,每组8只大鼠。ANP组大鼠采取逆行胰胆管注射5%牛磺胆酸钠制备ANP模型,各组大鼠于造模后相应时间点通过下腔静脉采取血液,随后摘取胰腺和垂体组织。全自动生化仪检测大鼠血清淀粉酶(AMY)、脂肪酶(LIP)水平,放射免疫分析法测定血清生长激素(GH)、促肾上腺皮质激素(ACTH)、促甲状腺激素(TSH)及促卵泡激素(FSH)水平,光镜下观察胰腺组织、垂体组织的病理学改变并比较组间差异。结果:N组与SO各组相比,除ACTH外,其余各指标差异均无统计学意义(P0.05);与N组和SO各组比较,ANP各组相应时间点血清AMY、LIP水平明显升高(P0.05);血清GH水平差异无统计学意义(P0.05);6h和12h组ACTH、TSH水平明显降低(P0.05),1h和3h组ACTH、TSH水平无统计学差异(P0.05);1h、6h和12h组FSH水平明显降低(P0.05),3h组FSH水平差异无统计学意义(P0.05)。光镜下,ANP 12h组胰腺病理损伤较SO 12h组明显加重(P0.05),且ANP 12h组垂体组织充血情况较SO 12h组明显加重(P0.05)。结论:ANP时,除胰腺外,大鼠垂体组织亦出现损伤及功能改变。     

急性坏死性胰腺炎血液流变学改变与治疗

目的通过纠正血液流变学异常，以期阻断胰腺炎不断恶化的病理过程。方法胰胆管注射牛磺胆酸制备大鼠急性胰腺炎模型，术后随机分别输注葡聚糖、生理盐水及葡聚精＋地塞米松。总液量控制在 ６ｍｌ／ｈ，共治疗３小时后，检测血液流变学指标、红细胞脆性试验和胰腺病理学改变。结果急性胰腺炎大鼠全血粘度、血浆粘度、红细胞压积均显著升高，纤维蛋白原降低，红细胞脆性增加。葡聚糖可显著降低急性胰腺炎大鼠的血液粘度、红细胞压积和红细胞脆性，并降低胰腺组织的炎症程度。结论 急性胰腺炎时血液流变学出现显著改变，葡聚糖可通过纠正血液流变学异常降低胰腺组织的炎症程度。     

Changes of Inflammation and Apoptosis in Adrenal Gland After Experimental Injury in Rats with Acute Necrotizing Pancreatitis

We hypothesize that adrenal insufficiency in acute necrotizing pancreatitis (ANP) is attributable to hemorrhagic inflammation, necrosis, and apoptosis of the adrenal cortex. Arguments to support this view are presented in the study that investigated morphological and functional changes of adrenal and the distinct roles of inflammatory mediator secretory phospholipase A₂ (sPLA₂) and apoptosis-related genes Bax and Bcl-2 played in acute adrenal injury in ANP. After ANP model was induced, pancreatic histology, serum amylase, sPLA₂, and corticosterone were analyzed. The adrenal morphology, apoptotic cells by TUNEL assay, and ultrastructures were observed. sPLA₂-IIA and Bcl-2 and Bax expressions were detected by immunohistochemistry. Histopathologic grading of adrenal was higher in ANP group than in controls. Serum corticosterone was stimulated to maximal level at 3 h, then dropped to the bottom at 24 h (P < 0.05). Apoptotic index, sPLA2-IIA, and Bax expression were increased steeply after pancreatitis, and the Bax/Bcl-2 ratio was elevated gradually (P < 0.05). Sustained decrease in serum corticosterone level following adrenal injury during ANP appears to be, in part, due to the crucial roles of inflammation and apoptosis in adrenal cortex. These findings could suggest that sPLA2, Bax, and Bcl-2 may be involved in the course of adrenal injury after ANP.     

瑞香素预处理对重症急性胰腺炎大鼠的抗氧化保护作用

目的:观察瑞香素预处理对重症急性胰腺炎(SAP)大鼠胰腺组织中丙二醛(MDA)和髓过氧化物酶(MPO)活性及一氧化氮(NO)的影响,探讨瑞香素在SAP中的抗氧化保护作用。方法:雄性Wistar大鼠72只,随机分为四组:假手术组(SO组)、SAP组、瑞香素预处理组(D-SAP组)、瑞香素药物对照组(D-SO组),每组18只。各组均用10%水合氯醛腹腔注射麻醉(0.3ml/100g)。SAP组和D-SAP组采用5%牛磺胆酸钠(1ml/kg)沿胰胆管逆行穿刺注射建立SAP模型。SO组和D-SO组与SAP造模程序相同,但用等量生理盐水代替5%牛磺胆酸钠注入胰胆管。D-SAP组和D-SO组于手术前30min给予瑞香素4mg/kg腹腔内注射。分别在术后3、6、12h分批处死各组大鼠各6只,检测血清淀粉酶(AMY)、脂肪酶(LIP)活性和胰腺组织MDA、MPO活性及NO含量,并进行HE染色观察大鼠术后12h时胰腺病理损伤程度。结果:D-SAP组大鼠血清AMY、LIP活性以及胰腺组织MDA含量、MPO活性和病理学评分较SAP明显降低(P0.01),但NO水平较SAP组明显升高(P0.01),SO组与D-SO组间各指标无统计学差异(P0.05)。结论:瑞香素预处理对SAP大鼠胰腺损伤具有明显的抗氧化保护作用。     

川芎嗪对急性胰腺炎大鼠细胞凋亡的影响

目的:研究川芎嗪(TMP)对急性胰腺炎(AP)血栓形成、组织病理变化、氧自由基和细胞凋亡的影响机制。方法:采用十二指肠胆胰管逆行加压注射5%牛磺胆酸钠的方法制备大鼠AP模型,动态观察TMP治疗前后大鼠血栓烷A2/前列环素代谢产物血栓烷B2/6-酮-前列腺素F1α(TXB2/6-Keto-PGF1α)比值(T/P)、血浆超氧化物岐化酶(SOD)、丙二醛(MDA)、淀粉酶(AMY)等各项指标;通过观察胰腺组织的病理形态进行病理评分;采用TUNEL法评价胰腺细胞凋亡指数(AI)。结果:经TMP治疗后,大鼠T/P值明显降低,血清SOD水平升高,MDA水平降低;胰腺组织病理评分为4.85±0.98(6h),AI为9.88±0.98(6h),与AP组比较差异有显著性意义(P<0.05)。结论:TMP对AP的治疗作用与其纠正血栓烷A2/前列环素I2失衡,改善AP大鼠微循环,减少自由基造成的损伤,诱导细胞凋亡,减少胰腺细胞坏死有关。     

Oxymatrine Ameliorates l-Arginine-Induced Acute Pancreatitis in Rats

The aim of this study was to determine whether oxymatrine has a protective effect against acute pancreatitis (AP) in a rat model of l-arginine-induced AP. AP was induced by two intraperitoneal injections of l-arginine (250 mg/100 g) at a 1-h interval. Oxymatrine (50 mg/kg) was administered every 6 h after the induction of AP. Oxymatrine significantly reduced the plasma amylase, d-lactic acid and tumor necrosis factor alpha concentration, serum diamine oxidase and lipase activity, and pancreatic myeloperoxidase activity, which were increased in AP rats (P < 0.05). In addition, the pancreatic CD45 expression and the expression of claudin-1, but not zonula occludens-1 (ZO-1) and occludin, in the intestinal tissues were significantly reduced after the induction of AP. However, oxymatrine increased the expression of claudin-1 and CD45, but did not alter the expression of ZO-1 and occludin. In conclusion, our results demonstrated that oxymatrine is potentially capably of protecting against l-arginine-induced AP and attenuating AP-associated intestinal barrier injury by up-regulation of claudin-1.     

生长抑素类似物对急性胰腺炎大鼠胰腺微血流的影响及作用

在５％牛磺胆酸钠诱导的大鼠急性出血坏死性胰腺炎（ＡＨＮＰ）模型上应用胰酶分泌抑制剂ＳＭＳ２０１－９９５（一种生长抑素类似物）防治，并观察其对ＡＨＮＰ时平均动脉压、胰腺微区血流量、血清淀粉酶和脂肪酶及胰腺病理形态的影响。发现ＳＭＳ２０１－９９５对大鼠ＡＨＮＰ时平均动脉压早期无明显影响，１２０ｍｉｎ后有所改善；能显著地降低血清淀粉酶和脂肪酶及减轻胰腺炎的病理学严重程度，并进一步增加胰腺微区血流量。表明ＳＭＳ２０１－９９５通过抑制胰酶释放能有效地防治胰腺炎和改善胰腺微血流，同时也说明胰腺炎时胰腺微循环障碍与大量胰酶释放入血有关     

实验性急性坏死性胰腺炎狗血液粘弹性改变

为研究血液流变学在急性出血性坏死性胰腺炎(AHNP)发病机理中的作用,将44条杂种狗分成5组。第Ⅰ、Ⅱ组分别为手术对照组和急性间质性胰胰炎组(两组各有8条狗)。第Ⅲ、Ⅳ、Ⅴ组狗的主管内注入牛磺胆酸钠溶液形成实验性急性出血性坏死性胰腺炎。而第Ⅳ、Ⅴ组分别用低分子右旋糖酐40(DX40)和丹参溶液静脉注入作为治疗。在所有5组中动脉血压和中心静脉压于手术前后均未见显著性改变。第Ⅲ、Ⅳ、Ⅴ组的血清淀粉酶和脂肪酶水平在实验性AHNP形成后明显增高。但在第Ⅳ、Ⅴ组用药物治疗后,此两酶水平迅速降低。用Low Shear-30流变测定仪测定血液流变学改变。所有5组血浆粘度在手术前、后无明显变化。第Ⅰ、Ⅱ组狗全血的红细胞压积(HCT),在0.512秒~(-1)和51.2秒~(-1)下的表观粘度(η0.512,η51.2),红细胞聚集指数(AI),复粘度的粘性分量(η′)和弹性分量(η″)、以及弹性模量(G′)在手术前后均无明显改变。然而,上述这些参数在实验性AHNP形成后的第Ⅲ、Ⅳ、Ⅴ组有明显增高。但在第Ⅳ和Ⅴ组用药物治疗后,这些参数持续下降;而且,第Ⅴ组丹参溶液比第Ⅳ组的DX40对于血液流变学改变有更好的改善作用。结果证明血液流变学异常是AHNP时引起胰腺微循环障碍的重要因素,并且血液流变学异常的纠正能改善出血性坏死性胰腺炎的症状。     

Involvement of Interleukin-17A in Pancreatic Damage in Rat Experimental Acute Necrotizing Pancreatitis

Interleukin (IL)-17A is a proinflammatory cytokine, which has recently attracted much interest due to its pathogenic role in various inflammatory conditions such as ischemia/reperfusion injury, chronic inflammation, and autoimmune diseases, but the role of IL-17A in acute pancreatitis remains unclear. This study aimed to investigate the role of IL-17A in experimental acute necrotizing pancreatitis (ANP). We analyzed the expression of IL-17A during the pathogenesis of ANP in vivo induced by 3 % sodium taurocholate (NaTc), by microarray test, quantitative real-time PCR, Western blotting, enzyme-linked immunosorbent assay, and immunohistochemistry. The effects of IL-17A on pancreatic acinar cells and pancreatic stellate cells (PSCs) were further investigated in vitro using recombinant rat IL-17A (rIL-17A). Expression of IL-17A was significantly increased following experimental acute pancreatitis. In addition, rIL-17A induced rat pancreatic acinar cell necrosis and promoted expression of several target genes, including IL-6, IL-1β, CXCL1, CXCL2, and CXCL5, in acinar cells and PSCs. These findings suggest that IL-17A may be involved in pancreatic damage by regulating the expression of inflammatory cytokines and chemokines during experimental acute pancreatitis.     

血液灌流对重症急性胰腺炎大鼠血液中细胞因子的影响

观察血液灌流对重症急性胰腺炎(SAP)大鼠血液中细胞因子的影响.方法:采用经胰管注射牛黄胆酸钠制造大鼠SAP模型,用NK-107树脂对SAP大鼠行血液灌流并测定血液中白细胞介素1(IL-l)、白细胞介素6(IL-6)及肿瘤坏死因子(TNF)的变化情况.结果:SAP大鼠血液中的IL-1、IL-6、TNF在发病早期可明显升高,通过血液灌流可使这些细胞因子的水平下降.从而使SAP大鼠的病死率由53.33%降至25.93%,存活时间平均由24.20±5.60小时延长至30.50±630小时.结论:NK-107树脂血液灌流对SAP有一定治疗作用.     

N-乙酰半胱氨酸对重症急性胰腺炎大鼠肺损伤作用的实验研究

目的:探讨N-乙酰半胱氨酸(NAC)对重症急性胰腺炎(SAP)大鼠肺损伤的作用。方法:雄性SD大鼠30只,随机分为假手术组(SO组)、SAP组、NAC组。胆胰管逆行注射5%牛磺胆酸钠制备SAP模型,造模后30min腹腔注射5%NAC(0.2ml/100g)干预SAP模型,12h后处死大鼠。检测各组血清淀粉酶(AMY)、肺组织髓过氧化物酶(MPO)、胰腺和肺组织病理学评分、肺组织肿瘤坏死因子-α(TNF-α)和细胞间粘附分子-1(ICAM-1)mRNA表达的变化。结果:与SO组比较,SAP组AMY、MPO、胰腺和肺组织病理学评分明显升高(P<0.01),TNF-α和ICAM-1mRNA表达明显增强(P<0.01);应用NAC处理后,AMY和MPO水平下降,胰腺和肺组织损伤缓解,TNF-α和ICAM-1mRNA表达减弱,与SAP组有明显差异(P<0.01)。结论:NAC对SAP大鼠肺损伤具有保护作用,其机制可能与抑制肺组织TNF-α和ICAM-1mRNA的表达有关。     

Baicalin Protects Thymus of Rats with Severe Acute Pancreatitis

To study the protective role of Baicalin on rats thymus with severe acute pancreatitis (SAP). The SAP rats were randomly assigned to the model control, Baicalin treated and Octreotide treated groups. Normal rats were assigned to the sham-operated group. The rat survival rates, pathological changes of thymus, apoptotic indexes and expression levels of NF-κB, Bax, Bcl-2, Caspase-3 and P-selectin of all groups were observed and recorded at 3, 6 and 12 h after operation, respectively. Rat survival rates were significantly higher in both Baicalin- and Octreotide-treated groups than those in the model control group at 12 h (P?<?0.05). The thymus pathological score was significantly lower in Baicalin treated group than in control group at 3 and 12 h (P?<?0.05). The expression of NF-κB, Bax and Bcl-2 in thymus tissue was negative in all groups. At 3 h after operation, the staining intensity, positive staining rate and intensity of Caspase-3 protein in the thymuses of the Baicalin treated group were significantly higher than those in the model control group (P?<?0.01). At different time points after operation, no marked difference was observed in the staining intensity of P-selectin protein between the Baicalin treated group and the model control group (P?>?0.05). At 6 h after operation, the positive staining rate and intensity of P-selectin protein in the Baicalin treated group was significantly lower than those in the model control group (P?<?0.05). The apoptotic indexes were significantly higher in treated group than in model control group at 6 h (P?<?0.05). Baicalin has a protective role on the thymus of SAP rats, and its effect of decreasing inflammatory mediators level in blood, inhibiting P-selectin expression and inducing apoptosis of thymocytes may involve in the mechanism of its protective role.     

Effect of Emodin on Endoplasmic Reticulum Stress in Rats with Severe Acute Pancreatitis

This study aimed to investigate the protective effect of emodin on endoplasmic reticulum (ER) stress in rats with severe acute pancreatitis (SAP) and the underlying molecular mechanism. Sprague–Dawley male rats were randomly divided into sham operation group, SAP model group, and emodin treatment group. SAP was constructed through injecting sodium taurocholate into pancreatic and biliary duct in rats. Half an hour before establishing the animal model, emodin or sodium carboxymethylcellulose was intragastrically administrated to the rats in respective group. Rats were killed at 3, 6, and 12 h postdisease induction. The amylase, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) levels in serum, pancreatic histopathology, acinar ER ultrastructure, protein expression of Bip, IRE1α,TRAF2, ASK1, p-JNK, and p-p38 MAPK in pancreas were examined. Sodium taurocholate induced pancreatic injury and ER lumen dilated in exocrine pancreas in rats at 3-, 6-, and 12-h time points. ER stress transducers Bip, IRE1α, and their downstream molecules TRAF2, ASK1 in pancreatitis were upregulated. Furthermore, phosphorylation of JNK and p38MAPK in pancreas was increased, which induced high expression level of inflammatory cytokines such as TNF-α and IL-6. Treatment with emodin obviously ameliorated pancreatic injury and decreased the release of amylase and inflammatory cytokines. Further studies showed that emodin significantly decreased the expression of Bip, IRE1α, TRAF2, and ASK1, inhibited phosphorylation of JNK and p38 MAPK in pancreas in rats at all time points. Emodin could reduce pancreatic injury and restrain inflammatory reaction in SAP rats partly via inhibiting ER stress transducers IRE1α and its downstream molecules.     

Effects of Dexamethasone and Salvia miltiorrhizae on the Small Intestine and Immune Organs of Rats with Severe Acute Pancreatitis

To observe the protecting effects and mechanisms of Dexamethasone and Salviae miltiorrhizae on intestinal mucosa and immune organs (spleen, thymus and lymph node) in rats with severe acute pancreatitis (SAP). The rats were randomly divided into sham-operated, model control, Dexamethasone treated group and Salviae miltiorrhizae treated group. At 3, 6 and 12 h after operation, the mortality rate, pathological changes of intestinal mucosa and immune organs as well as the contents of serum PAF, IL-1β and sIL-2R were observed, respectively. The mortality rate and the contents of PAF (at 3 and 6 h), IL-1β (at all time points) and sIL-2R (at 3 and 6 h) as well as the pathological scores of thymus (at all time points) and spleen (at 3 h) in Dexamethasone treated group were significantly lower than those in model contrlo groups (P < 0.05). The contents of PAF (at 3 and 12 h), IL-1β (at 6 and 12 h) and sIL-2R (at 3 and 6 h) as well as the pathological scores of thymus (at all time points) and spleen (at 3 and 12 h) in Salviae miltiorrhizae treated group were markedly lower than those in model contrlo groups (P < 0.05). Since both Dexamethasone and Salvia miltiorrhizae can reduce the contents of serum PAF, sIL-2R and IL-1β, mitigate the pathological changes in the small intestine, spleen and thymus and reduce the mortality rate of SAP rats, they show good therapeutic effects on SAP rats.     

益活清胰Ⅰ号对重症急性胰腺炎大鼠中性粒细胞与内皮细胞黏附的抑制作用

目的观察益活清胰Ⅰ号对重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠的中性粒细胞(polymorphonuclear cell,PMN)-内皮细胞(endothelial cell,EC)黏附率及PMN表面黏附分子CD11/CD18表达的影响,探讨其治疗SAP的机理。方法81只SD大鼠随机分为假手术组(n=27)、造模组(n=27)、治疗组(n=27),SAP模型采用5%的牛磺胆酸钠胰胆管逆行注射方法建立。6、12、24h分批处死动物9只采集动脉血和胰腺组织标本,测定胰腺组织的MPO活性,HE染色光镜下观察胰腺组织的病理变化。分离PMN,与体外培养的血管内皮细胞作用测定PMN-EC黏附率,ELISA法测定PMN表面CD11a/CD18、CD11b/CD18。结果与假手术组比较,造模组和治疗组术后各时点胰腺组织MPO活性、PMN-EC黏附率、PMN表面CD11a/CD18和CD11b/CD18均增高(P<0.01),治疗组术后各时点胰腺组织MPO活性、PMN-EC黏附率、PMN表面CD11a/CD18和CD11b/CD18均显著低于造模组(P<0.01)。造模组胰腺组织出血和坏死严重,治疗组的病理损伤明显减轻。结论益活清胰Ⅰ号能降低PMN表面CD11a/CD18和CD11b/CD18的表达水平,减轻PMN与EC的黏附,从而有助于减轻PMN与EC黏附所致的胰腺组织病理损伤。     

丹参注射液对高脂血症合并重症急性胰腺炎大鼠胰腺血流量和组织病理改变的影响

目的:观察丹参注射液对高脂血症合并重症急性胰腺炎大鼠(SAP)胰腺局部血流量和组织病理改变的影响。方法:32只雄性SPF级大鼠随机分为普通饮食空白组(SO组,普通饲料喂养)、高脂血症组(HL组,高脂饮食喂饲建立高脂血症模型)、高脂+SAP组(HAP组,高脂血症模型建模成功后再建SAP模型)、高脂+SAP+丹参治疗组(SM组,在HAP组基础上加用丹参注射液干预),每组各8只大鼠。应用多普勒超声检测系统测定各组胰腺局部血流量,下腔静脉取血测定各组血清甘油三酯(TG)、总胆固醇(TC)及淀粉酶(AMY)水平,取各组大鼠胰腺行HE染色,观察组织病理学改变,并行病理评分。结果:HL组大鼠胰腺局部血流量明显低于SO组,HAP组更低(P0.01),而SM组明显高于HAP组(P0.01)。HL组和/或HAP组大鼠AMY、TC、TG水平明显高于SO组,SM组则显著降低(P0.01)。HL组和HAP组胰腺组织分别出现脂肪组织增生、腺泡坏死、出血及炎性细胞浸润、胰腺病理评分显著升高(P0.01),而SM组的上述病理组织学变化缓解,胰腺病理评分也明显下降(P0.01)。结论:丹参注射液能够改善高脂血症合并SAP大鼠的胰腺血流状况和组织病理学变化。     

重症急性胰腺炎大鼠肾上腺病理及超微结构变化

目的:观察重症急性胰腺炎(SAP)大鼠肾上腺皮质的病理和超微结构变化。方法:采用5%牛磺胆酸钠逆行胰管注射法建立SAP模型,分别于术后3、12、24h测定血淀粉酶,观察胰腺、肾上腺皮质病理变化,透射电镜观察12h肾上腺皮质束状带细胞超微结构。结果:SAP造模成功后,血淀粉酶、胰腺病理评分进行性升高。3h时肉眼见肾上腺包膜轻度水肿,并逐渐加重,24h最为明显;3h肾上腺组织出现血窦扩张,12h可见肾上腺组织水肿、腺体结构轻度破坏、少量炎性细胞浸润,24h肾上腺皮质部分细胞变性及出血性坏死,腺体结构破坏严重;12hSAP大鼠肾上腺皮质束状带细胞超微结构损伤和分泌功能降低等改变。结论:随着SAP病情进展,肾上腺组织病理及超微结构损害加重。肾上腺功能减退可能与其病理、超微结构损伤有关。     

急性胰腺炎大鼠胰腺血流量与蛋白酶-抗蛋白酶平衡的关系

本文观察了大鼠急性性胰腺炎(AP)时胰腺供血以及血浆胰蛋白酶与α_2-巨球蛋白(α_2-M)的变化。发现AP时胰腺血流量(％心输出量)与胰腺组织灌流量(血流量/g胰腺组织)明显减少;血浆胰蛋白酶活力明显增高,而α_2-M水平明显降低。还发现胰腺供血的变化与胰蛋白酶/α_2-M比率的变化呈负相关。提示AP时血浆蛋白酶-抗蛋白酶失衡与胰腺缺血有关。