Delayed Gastrointestinal Transit And Changes Of Myenteric Nerve Plexus In Severe Acute Pancreatitis Rat Complicated With Hyperlipemia.

Objective:To build a rat model of hyperlipemia(HL) and severe acute pancreatitis (SAP).To investigate the relation between the delayed gastrointestinal transit and the changes of myenteric nerve plexus,throught observing the changes of gastrointestinal transit and myenteric nerve plexus in SAP rats and those complicated with hyperlipemia.To further explore the formed mechanism of gastrointestinal motility dysfunction.Method: Male Sprague-dawley(SD) rats(40) were divided into four groups:nomal control group, SAP group, HL control group and HL+SAP group.The specific methods are as follows:First,the rats were randomly divided into two groups(N=20),respectively feeding normal diet and high-fat diet (which consist of 88%nomal diet , 10% lard and 2% cholesterol) for 4 weeks.After 4 weeks, each group was randomly devided into two groups(n=10) again, SAP group and sham operation group. Each used retrograde injection 3.5% sodium taurocholate which induced severe acute pancreatitis and NS into the pancreatic duct respectively. Materials were gained after six hours the models was building successfully.To observed the histopathologic damage degree of pancreas and measure the value of amylase (AMS),triglyceride (TG),total cholesterol (TC) in serum to judge if the model was builded successfully or not. Gastrointestina1 transit distance was measured by ink gavage and histologic changes of cholinergic and nitriergic nerves in myenteric plexus were observed with enzymatic histochemistry. method of Karnovsky-Root and NADPH.Results: The level of HL, TG and CH in serum of HL group is higher than the controlled group(P=0.0001﹤0.01), the level of AMS in serum of SAP group is higher than the controlled group(P=0.0001﹤0.01).And pancreas is found to get worse bleeding and necrosis histopathologic change,gastrointestinal transit distance was found delayed(P=0.003﹤0.01) comparing with control group.The density of cholinergic neurons in the ileum myenteric plexus were decreased(P=0.0001﹤0.01)and the densities of nitriergic ganglions and neurons were significantly increased comparing with control group(P=0.0001﹤0.01).The same situation was found in SAP rat complicated with HL.comparing with control group. the level of AMS in serum of SAP+HL group is lower than the SAP group(P=0.0001﹤0.01),have more damage in pancreas(P=0.0001﹤0.01). gastrointestinal transit distance was found delayed comparing with SAP group(P=0.0001﹤0.01) .The density of cholinergic neurons in the ileum myenteric plexus was decreased(P=0.042﹤0.05)and the densities of nitriergic ganglions and neurons were significantly increased comparing with SAP group(P=0.005﹤0.01), and the two index had linear regression relation(R2=0.531, P=0.001﹤0.01)Conclusion: An ideal animal model.of hyperlipemia can be builded by feeding high-fat diet for 4 weeks.A model of severe acute pancreatitis complicated with hyperlipemia in rat might be developed by feedinghigh-fat diet for 4 weeks and retrograde injection of 3.5% sodium taurocholate into the pancreatic duct. In the early stage of SAP, there are significantly gastrointestinal transit delayed in the SAP rats.,Decrease of cholinergic nerves and increase of nitriergic nerves in the myenteric plexus of intestine might be the nerve mechanisms of delayed gastrointestinal transit distance in SAP rats. Hyperlipemia can aggravate the progress of pancreas damage and delayed gastrointestinal transit in SAP rats.The increase of nitriergic nerves play an more important role in the progress of delayed gastrointestinal transit. Gastrointestinal dynamic disorder which induced enterogenous infection may be one mail factor of HL aggravate the progress of SAP.