Objective To evaluate the predicted value of APACHEⅡ score at admission for deep fungal infection（DFI） in patients with severe acute pancreatitis （SAP）.Methods The clinical data of 132 patients with SAP from January 2006 to June 2011 in our hospital were analyzed retrospectively. The receiver operating characteristic curve （ROC） was used for evaluating the predicted value.Results Thirty-nine patients with SAP infected DFI （29.5%）,of which 36 patients （92.3%） infected with Candida albicans,2 patients （5.1%） with Candida tropicalis,1 patient （2.6%） with pearl bacteria.And,among these 39 patients,27 patients （69.2%） infected at single site,12 patients （30.8%） infected at multi-site. The APACHEⅡ score in 39 patients with DFI was higher than that of 93 patients without DFI （17.1±3.8 versus 9.7±2.1, t=14.316,P=0.000）.The ROC for APACHEⅡ score predicting DFI was 0.745（P=0.000）, 95%CI was 0.641－0.849.When the cut off point was 15,it showed the best forecast performance,with specificity 0.81, sensitivity 0.72,Youden index 0.53. Conclusions The APACHEⅡ score at admission can preferably predict DFI in patients with SAP； when the APACHEⅡ score is greater than 15,it prompts highly possible of DFI,so preventive anti-fungal treatment may be necessary.
OBJECTIVE To observe the effects of basic fibroblast growth factor (bFGF) on repairing injury of intestinal mucosa in acute necrotic pancreatitis (ANP). METHODS Sixteen dogs of ANP animal model were made by injection of 5% sodium taurocholate (0.5 ml/kg) with 3,000 U/kg trypsin into the pancreatic duct. The mucosa structure, content of protein, DNA and malondiethylaldehyde (MDA) were observed after ANP and treatment with bFGF, and the plasma lipopolysaccharide and endothelin-1 were detected. The organs of dogs were made to bacterial culture. Ileal mucosa was collected for histological and ultrastructural studies. RESULTS The results showed that after treatment with bFGF, the injury of intestinal mucosa in ANP was abated. The length, height and area of mucosa microvillus, the content of DNA and protein of ileal mucosa were significantly increased, while the plasma endothelin-1 and lipopolysaccharide were reduced. The organ bacterial translocation rate was also decreased in 50%. CONCLUSION bFGF has good effects on abating injury of intestinal mucosa, protecting gut barrier function, reducing the incidence of lipopolysaccharide and bacterial translocation after ANP.
The aim of this study was to investigate the role of tumor necrosis factor (TNF), interleukin-6(IL-6), C-reactive protein (CRP) in pancreatitis and its systemic complications. Thirty six patients with acute pancreatitis were studied, 12 with mild disease, and 24 severe disease, of whom 9 developed systemic complications. TNF, IL-6, CRP in these patients with pancreatitis was assessed during the first, 4th, 8th days of admission. The serum concentration of TNF, IL-6, CRP were significantly increased, and significantly higher in complicated group than in mild group and severe group. These findings suggest that proinflammatory cytokines play a central role in the pathophysiology of the disease, the host systemic response to pancreatic inflammation and the level of the response did relate to the development of organ dysfunction.
Objective To investigate the relationship between gene expression of endothelin-3 (ET-3） and inflammation of acute pancreatitis （AP） in rats. Methods Fifty-four rats were divided randomly into 4 groups: sham operation group, AP group, arterial injection group and vein injection group. AP was induced by reverse intra-bile duct infusion 4.5% sodium taurocholate, treated with low dose dopamine 〔5 μg/（kg·min）〕 by injecting arterial or tail vein. Rats were sacrificed at 1， 6 and 24 h after the induction of AP. The mRNA expression of ET-3 was evaluated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and pathological changes was observed in rats. Results Expression of ET-3 mRNA could be detected from 1 up to 24 h after the induction of pancreatitis. Expression of ET-3 mRNA of sham operation group was decreased significantly compared with other three groups. Expression of ET-3 mRNA showed a significant decrease by arterial injection dopamine than that by tail vein (P＜0.05， P＜0.01). The pathologic score in AP group was the highest, vein injection group was the next one, and score in sham operation group was the lowest. Conclusion There are significant relationship between inflammation of AP and expression of ET-3 mRNA. Dopamine administration by arterial injection is more effective than that by tail vein injection.
Objective To study the effects of endothelin (ET) on acute pancreatitis in rats. Methods The acute edematous pancreatitis (AEP) and hemorrhagic necrotizing pancreatitis (AHNP) model of rats were induced by cerulein and dextran-110 and endothelin-1 was administered on AEP rats via intravenous injection. Serum amylase, plasma ET and 6-Keto-PGF1α, pancreas hostologic observation were determined. Results The serum concentration of amylase increased markedly in AHNP rats, and there was a significant difference between AHNP and AEP (Ｐ＜0.01). A dose of extrinsic ET-1 may induce the conversion of AEP to AHNP in rats. The degree of pancreatic damage correlates positively with the level of the plasma ET. Conclusion Endothelin might take part in the development of acute pancreatitis, and play a key role in the conversion of AEP to AHNP.
Objective To explore the effect of artemisinin on the apoptosis of pancreas acinar cells in acute pancreatitis (AP), and to study whether artemisinin can relieve the severity of AP. Methods ① In vivo experiment: twenty one Wistar rats were divided into the following 3 groups randomly: the normal control group, the AP group and the artemisinin group. The model of AP was established by injecting cerulein into the peritoneal cavity of rat. After establishment of AP in the artemisinin group, artemisinin was injected into the peritoneal cavity. Meanwhile normal saline was injected into the peritoneal cavity of rats of the normal control group and the AP group. The apoptosis of pancreas acinar cell was detected by terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL). The activity of myeloperoxidase was detected by absorption spectrometry. ② In vitro experiment: the pancreas acinar cells of normal rats were isolated through twostep enzyme digestion, and cultured. These acinar cells were divided into 3 groups: the normal control group, the AP group and the artemisinin group. Then, the cells of AP group were cocultured with cerulein, and those of the artemisinin group were cocultured with cerulein and artemisinin. The apoptosis of pancreas acinar cells were detected by AO dyeing and the measurement of the activity of caspase3. And the activity of LDH and AMS in the culture medium of each group were measured. Results ① In vivo: the apoptosis index of the artemisinin group was sigificantly increased and the activity of myeloperoxidase was obviously decreased compared with the AP group (P＜0.05). ② In vitro: the apoptosis index and the activity of caspase3 of the artemisinin group were significantly increased compared with the AP group (P＜0.05); the activities of LDH and AMS of the artemisinin group were more decreased than those of the AP group (P＜0.05). Conclusion Artemisinin could contribute to the apoptosis of rat pancreas acinar cells, decrease the releasing of trypsogen, alleviate the activation of neutrophil and relieve the severity of AP.
In order to choose the appropriate antibiotics for treating secondary pancreatic infection, permeability of antibiotics to pancreatic tissue was investigated on experimental dogs with acute hemorrhagic necrotizing pancreatitis. The concentrations of 8 different antibiotics were determined in the blood and the pancreatic tissue using highperformance liquid chromatography. Pancreatic tissue permeability of Cefotaxime, Ofloxacin, Amikacin, Piperacllin, Cefoperazone, Ampicillin, Metronidazole and Ciprofloxacin was 12%, 19%, 20%, 46%, 55%, 63%, 71% and 132% respectively. The study shows that this eight antibiotics have different permeability to the pancreatic tissue. Such observations support the existence of a bloodpancreas barrier, which acts to restrict the permeation of antibiotics into the pancreas. The results suggest that antibiotics with high permeability rate be used to treat the patient with secondary pancreatic infection.
【Abstract】Objective To investigate the role of interleukin-10（IL-10） and interleukin-18 （IL-18） in the pathogenesis of acute lung injury in experimental severe acute pancreatitis.Methods Forty-eight SD rats were divided into control group and SAP group by the random data table. The model of experimental severe acute pancreatitis was established by injection of 3.5% sodium taurocholate into the bili-pancreatic duct. Lung wet weight index, ascities and level of serum amylase, IL-10 and IL-18 were quantitatively measured in different time. Intrapulmonary expressions of IL-10 mRNA and IL-18 mRNA were detected by semiquantitative RTPCR. The histopathology of pancreas and lung were observed under the light microscope.Results Lung wet weight index, ascities, level of serum amylase, IL-10 and IL-18, intrapulmonary expressions of IL-10 mRNA and IL-18 mRNA were significantly increased in SAP group (P＜0.01). The level of serum IL-18 and intrapulmonary expression of IL-18mRNA are positively correlated with lung wet weight index （r=0.68,P＜0.01; r=0.72,P＜0.01） and lung injury score （r=0.74,P＜0.01; r=0.79,P＜0.01) respectively, whereas the level of serum IL-10 and intrapulmonary expression of IL-10 mRNA are negatively correlated with lung wet weight index（r=-0.62,P＜0.01; r=-0.69,P＜0.01） and lung injury score（r=-0.66,P＜0.01; r=-0.60,P＜0.01）. Conclusion IL-18 may play a key role in the pathogenesis of acute lung injury in experimental severe acute pancreatitis, and IL-10 exerts the protection role in this process.
This study aimed to assess the therapeutic effect of mannital administration on acute hemorrhagic necrotizing pancreatitis (AHNP), 28 Wistar rats were randomily divided into therapeutic group and control group after induction of AHNP by retrograde intraductal injection of 5 percent sodium taurocholate. The rats of therapeutic group received intravenous 20% mannital (1g/kg) through tail vein, once in 12 hours, until the end of experiment; control group received saline (5.0 ml/kg) with the same way. Blood of all the rats were collected from heart and the rats were killed after 96 hours. Results: lipid peroxide (LPO) in pancreatic tissue, LPO in serum, lactate dehydrogenase (LDH), alpha-1-antitrypsin (α1-AT), glutamicoxalacetic transaminase (GOT), necrotizing square of pancreatic tissue in the therapeutic group were significantly less than those in control group (Ｐ＜0.05 or Ｐ＜0.01). The damage to pancrease, heart, liver, kidney in the therapeutic group were lighter than those of the control group and the mortality was lower (Ｐ＜0.05).Conclusions: Mannital can scavenge the oxygenderived free radicals and play a therapeutic role in AHNP.
【Abstract】ObjectiveTo investigate the effect of ischemia-reperfusion （I/R） injury on apoptosis of pancreatic cells in rats with acute pancreatitis(AP). MethodsFifty-four SD rats were randomized into 3 groups: pancreatitis group (n=24), I/R-injury group (n=24) and control group (n=6). The animal model of AP was induced by retrograde injection of 3% sodium taurocholate into biliopancreatic duct in rats. Pancreatic I/R was caused by blocking the inferior splenic artery and removing the clamp after AP induction. At 1 h, 3 h, 6 h and 12 h, groups of rats were sacrificed. A terminal deoxynucleotidyl transferase-mediated dUTP-biotion nick end labeling (TUNEL) was used to detect pancreatic apoptosis, and histological changes of the pancreas were observed. ResultsPancreatic hemorrhage, necrosis were respectively observed in the pancreatitis rats at 6 h and the I/R-injury rats at 1 h. Histological changes of the pancreatitis rats at 1 h and 3 h were only congestion and edema. Apoptoic acinar cells increased after AP induction, the peak respectively appeared at 6 h in the pancreatitis rats and at 3 h in the I/R-injury rats. Compared with the pancreatitis rats, apoptosis index (AI) of the I/Rinjury rats was significantly higher at 1 h and 3 h (P＜0.01, P＜0.05, respectively), but lower at 6 h and 12 h (P＜0.05, P＜0.01, respectively). ConclusionI/R injury can induce conversion of edematous pancreatitis to hemorrhagic necrotizing pancreatitis and apoptosis of acinar cells. Apoptosis may be a beneficial response to pancreatic injury in AP.