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Aim: To study retrospectively the influence of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) in patients with early acute pancreatitis (AP) (during the first week after admission) on physiological functions, and the association of the presence of IAH/ACS and outcome., Methods: Patients (n = 74) with AP recruited in this study were divided into two groups according to intra-abdominal pressure (IAP) determined by indirect measurement using the transvesical route via Foley bladder catheter during the first week after admission. Patients (n = 44) with IAP >or= 12 mmHg were assigned in IAH group, and the remaining patients (n = 30) with IAP < 12 mmHg in normal IAP group. For analysis of the influence of IAH/ACS on organ function and outcome, the physiological parameters and the occurrence of organ dysfunction during intensive care unit (ICU) stay were recorded, as were the incidences of pancreatic infection and in-hospital mortality., Results: IAH within the first week after admission was found in 44 patients (59.46%). Although the APACHE II scores on admission and the Ranson scores within 48 h after hospitalization were elevated in IAH patients in early stage, they did not show the statistically significant differences from patients with normal IAP within a week after admission (16.18 +/- 3.90 vs 15.70 +/- 4.25, P = 0.616; 3.70 +/- 0.93 vs 3.47 +/- 0.94, P = 0.285, respectively). ACS in early AP was recorded in 20 patients (27.03%). During any 24-h period of the first week after admission, the recorded mean IAP correlated significantly with the Marshall score calculated at the same time interval in IAH group (r = 0.635, P < 0.001). Although ACS patients had obvious amelioration in physiological variables within 24 h after decompression, the incidences of pancreatitic infection, septic shock, multiple organ dysfunction syndrome (MODS) and death in the patients with ACS were significantly higher than that in other patients without ACS (pancreatitic infection: 60.0% vs 7.4%, P < 0.001; septic shock: 70.0% vs 11.1%, P < 0.001; MODS: 90.0% vs 31.5%, P < 0.001; mortality: 75.0% vs 3.7%, P < 0.001)., Conclusion: IAH/ACS is a frequent finding in patients admitted to the ICU because of AP. Patients with IAP at approximately 10-12 mmHg and early signs of changes in physiologic variables should be seriously considered for urgent decompression to improve survival.

Aim: To investigate the etiology and clinical characteristics of severe acute pancreatitis (SAP) in elderly patients (> or = 60 years of age)., Methods: We reviewed retrospectively all the SAP cases treated in Xuanwu Hospital in Beijing between 2000 and 2007., Results: In 169 patients with SAP, 94 were elderly and 16 died. Biliary and idiopathic etiologies were the first two causes that accounted for over 90% of SAP in the elderly. Biliary, hyperlipemic and alcoholic etiologies were the first three causes in the young. The proportion of co-morbidity of cholelithiasis, biliary infection, hypertension and coronary heart disease in the aged was significantly higher than that in their young partners. The scores of APACHE II and Ranson were also significantly higher in the elderly except the CT score. Organ failures were more common in the elderly, but the local pancreatic complications were not different between the two groups. Mortality of the aged was correlated with the severity of SAP, multiple co-morbidity and incidence of multiple organ dysfunction syndrome (MODS). MODS was the main cause of death., Conclusion: The etiology of SAP in the elderly is quite different from that in the young. Biliary and unknown factors are main causes in the aged. The elderly are subject to major organ failures but there is no difference in the occurrence of local pancreatic complications between the elderly and the young. It is crucial to monitor and improve the functions of major organs so as to prevent MODS in the aged with SAP.

Aim: To investigate the effects of hyperlipidemia on acute pancreatitis (AP) and the possible mechanisms., Methods: Rat models of hyperlipidemia and AP were established by Triton WR1339 and cerulein respectively. Human albumin was used to treat AP complicated by hyperlipidemia. In each group, we compared the histological score, volume of ascites, ratio of pancreatic wet/dry weight, serum amylase (AMY) and pancreatic acinar cell apoptosis. The level of protein kinase C (PKC) membrane translocation in pancreatic tissue was detected by Western blot., Results: In the hyperlipidemia model established by Triton WR1339, triglyceride (TG) increased remarkably and reached its peak 6 h after injection, and most rats developed mild acute pancreatitis. Histological score, volume of ascites, ratio of wet/dry weight and serum AMY in AP animals with hyperlipidemia were obviously higher than those in AP animals (P < 0.05) and decreased after albumin therapy but not significantly (P > 0.05). Apoptotic cells detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) increased in AP animals with hyperlipidemia and did not change distinctly after albumin therapy. PKC membrane translocation level increased in AP animals with hyperlipidemia and decreased remarkably after albumin therapy (P < 0.05)., Conclusion: Hyperlipidemia may induce AP or intensify pancreatic injury. Albumin therapy can not alleviate pancreatic lesion effectively. PKC activation may be one mechanism by which AP is intensified by hyperlipidemia.

Aim: To discuss the changes of intestinal mucosal immune function in rats with experimental severe acute pancreatitis (SAP) and the regulatory effect of L-arginine., Methods: Male adult Wistar rats were randomly divided into pancreatitis group, sham-operation group, and L-arginine treatment group. Animals were killed at 24, 48, and 72 h after SAP models were developed and specimens were harvested. Endotoxin concentration in portal vein was determined by limulus endotoxin analysis kit. CD3+, CD4+, CD8+ T lymphocytes in intestinal mucosal lamina propria were examined by immunohistochemistry. Secretory immunoglobulin A (SIgA) in cecum feces was examined by radioimmunoassay., Results: Compared to the control group, plasma endotoxin concentration in the portal vein increased, percentage of CD3+ and CD4+ T lymphocyte subsets in the end of intestinal mucosal lamina propria reduced significantly, CD4+/CD8+ ratio decreased, and SIgA concentrations in cecum feces reduced at 24, 48, and 72 h after SAP developed. Compared to SAP group, the L-arginine treatment group had a lower level of plasma endotoxin concentration in the portal vein, a higher CD3+ and CD4+ T lymphocyte percentage in the end of intestinal mucosal lamina propria, an increased ratio of CD4+/CD8+ and a higher SIgA concentration in cecum feces., Conclusion: Intestinal immune suppression occurs in the early stage of SAP rats, which may be the main reason for bacterial and endotoxin translocation. L-arginine can improve the intestinal immunity and reduce bacterial and endotoxin translocation in SAP rats.

Aim: To investigate the effects of exogenous unsaturated fatty acids on calcium-activated potassium current (I(K(Ca))) in gastric antral circular myocytes of guinea pigs., Methods: Gastric myocytes were isolated by collagenase from the antral circular layer of guinea pig stomach. The whole-cell patch clamp technique was used to record I(K(Ca)) in the isolated single smooth muscle cells with or without different concentrations of arachidonic acid (AA), linoleic acid (LA), and oleic acid (OA)., Results: AA at concentrations of 2,5 and 10 micromol/L markedly increased I(K(ca)) in a dose-dependent manner. LA at concentrations of 5, 10 and 20 micromol/L also enhanced I(K(Ca)) in a dose-dependent manner. The increasing potency of AA, LA, and oleic acid (OA) on I(K(Ca)) at the same concentration (10 micromol/L) was in the order of AA>LA>OA. AA (10 micromol/L)-induced increase of I(K(ca)) was not blocked by H-7 (10 micromol/L), an inhibitor of protein kinase C (PKC), or indomethacin (10 micromol/L), an inhibitor of the cyclooxygenase pathway, and 17-octadecynoic acid (10 micromol/L), an inhibitor of the cytochrome P450 pathway, but weakened by nordihydroguaiaretic acid (10 micromol/L), an inhibitor of the lipoxygenase pathway., Conclusion: Unsaturated fatty acids markedly increase I(K(ca)), and the enhancing potencies are related to the number of double bonds in the fatty acid chain. The lipoxygenase pathway of unsaturated fatty acid metabolism is involved in the unsaturated fatty acid-induced increase of I(K(ca)) in gastric antral circular myocytes of guinea pigs.

Aim: To investigate the effect of gastrin on differentiation of IEC-6 cell line in vitro., Methods: IEC-6 cells were incubated with gastrin. On day 7 after treatment, cell morphology was examined by light microscope, and on day 20, the cellular ultrastructures were examined by electron microscope. After exposure to gastrin for 6 hours, villin mRNA was analyzed by reverse transcription-polymerase chain reaction, and on day 7, the expression of villin was examined by immunocytochemical analysis with laser confocal microscope., Results: After exposure to gastrin, IEC-6 cells showed differentiated phenotypes as villas enterocytes and contained an abundance of plasma, small nuclei with nucleoli, and were arranged regularly. There were numerous microvilli around edge of the cells, and several cells showed columnar structures. Villin mRNA expression in cytoplasm was increased in comparison with control., Conclusion: Differentiated characteristics of villus enterocytes and phenotypic changes of rat intestinal epithelial cells (IEC-6) are induced by gastrin, and the effects of gastrin are correlated to increased villin expression.