| Objective: Severe acute pancreatitis (SAP) is a common surgical emergency with many complications and high mortality. The incidence of SAP is rising in recent years. The main cause of death in SAP is multiple organ dysfunction syndromes (MODS). In ex-pancreatic organ injury, many studies focus on hepatic injury, pulmonary injury, renal injury and encephalic injury, yet there were few studies about myocardial injury. However, cardiovascular decompensation is the complication with the highest mortality in acute pancreatitis, though the interest on it is inadequate in clinical practice. The aim of this study was to investigate the relationship between tumor necrosis factor (TNF- α ) and myocardial injury induced by SAP and evaluate the feasibility of anisodamine on treatment of the myocardial injury.Material and Methods: 54 healthy male SD rats were randomly divided into three groups: control group (n=18), SAP group (n=18), and Ani group (n=18). SAP model in SAP group and Am group was produced by the method of Aho et al. Under anaesthesia ,a laparotomy was performed and 5% sodium taurocholate (1 ml/kg body weight ) was injected into biliopancreatic duct at a rate of 0.2 ml/min by microinfusion pump. Control group was injected by the equivalence normal saline (NS) with the same method as a control of sham operation. Anisodamine was administered to Ani group via intarperitoneal (I.P.) with the dosage ofl0mg/kg at 0.5, 6, and 12 hours after operation. Normal saline (NS) was given to control group and SAP group in the same way and the same time. The animals were sacrificed at 6, 12 and 24 hours after operation under sterile circumstance. The serum samples were collected and then stored at -70℃. Serum myocardial enzymogram including lactate dehydrogenase (LDH), creatine phosphokinase (CK), the isoenzyme of CK (CK-MB), aspartate aminotransferase (AST), and a -hydroxybutyrate dehydrogenase (HBDH) were detected by assays recommendated by International Federation of Chemistry Committee (IFCC). Serum TNF- a were detected by ELISA.Results: (1)Serum myocardial enzymogram: (1)Serum lever of LDH in SAP group was higher than that in control group 6 hours after the model was made (P<0.01), and remained to 24 hours; serum lever of LDH in Ani group was lower than that in SAP group at 6, 12, and 24 hours respectively (P<0.01). (2)Serum lever of CK in SAP group was higher than that in control group 6 hours after the model was made (P<0.01), and remained to 24 hours; serum lever of CK in Ani group was lower than that in SAP group at 6, 12, and 24 hours respectively (P<0.01, P<0.05 ). (3)Serum lever of CK-MB in SAP group was higher than that in control group 6 hours after the model was made (P<0.01), and remained to 24 hours; serum lever of CK-MB in Ani group was lower than that in SAP group at 6, 12, and 24 hours respectively (P<0.01, PO.05 ). (4) Serum lever of AST in SAP group was higher than that in control group 6 hours after the model was made (P<0.05), and remained to 24 hours (P<0.01); serum lever of AST in Ani group was lower than that in SAP group at 6, 12, and 24 hours respectively (P<0.01, P<0.05 ). (5)Serum lever of HBDH in SAP group was higher than that in control group 6 hours after the model was made(P<0.01), and remained to 24 hours; serum lever of HBDH in Ani group was lower than that in SAP group at 6, 12, and 24 hours respectively (P<0.01). (2)Serum lever of TNF-α in SAP group was higher than that in control group 6 hours after the model was made (P<0.01), and remained to 24 hours; serum lever of TNF- a in Ani group was lower than that in SAP group at 6, 12, and 24 hours respectively (P<0.01, P<0.05 ).Conclusion: 1. Myocardial injury is existent in rats with SAP. 2.The myocardial injury is related to the increasing serum lever of TNF- a induced by SAP in rats. 3. Anisodamine has therapeutic effects on myocardial injury induced by SAP in rats. 4. The therapeutic effects of anisodamine is related to the effect that it can reduce the serum lever of TNF- a induced by SAP in rats.
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