| Acute pancreatitis is a kind of common surgical acute abdomen. The edematous pancreatitis is self-limited, but part of patients may have developed rapidly into severe acute pancreatitis from local pancreatic inflammation with dangerous systemic inflammatory response and multiple system organ failure. The evolution process and developed triggers are complexed. Aside from pancreatic enzymes activiation and autodigestive process, recent investigations have established that the upregulation of inflammatory mediator are believed to be the critical steps in the progression of mild pancreatitis to severe pancreatitis. Tumor necrosis factor-(, ThyomboxaneA2 ,ProstaglandinsI2 are all important inflammatory mediator. TNF-( is one of cytokines. It is important to the over-production of ICAM-1,VCAM-1, TXA2 andPGI2. The ICAM-1 and VCAM-1 mediate both leukocytes adhesion and migration through the endothelium into tissues to connect with injuried target cells. The TXA2 and PGI2 are the production of arachidonic acid. They are responsible for the tissue ischaemia. Objective: By analyzing the changes of TNF-(,TXA2,PGI2 in experimental severe acute pancreatitis and kidney damage, To study the mechanism of pathophysiology of severe acute pancreatitis and kidney, Seek for a new efficient therapeutic method. Methods:168 Sprague-Dawley rats were randomly divided into 4 groups. Group A was the operation control group(n=24), Group B,C,D(each group animal numbers n=48) were all severe acute pancreatitis,The SAP model was esta- blished by injection of 5% sodium taurocholate(0.15ml/100g) under pancreatic capsule, Group C was therapeutic group with Ozagrel(2.5mg/100g )at one hour after induction of pancreatitis, Group D was the therapeutic group with 0.9% normal saline。Animals were killed at3,6,12hours and before death(Group A n=6 at each time point, Group B,C,D n=12 at each time point ).The serum, plasma, and pancreas, kidney were reserved, the variation of inflammatory mediators (TNF-(,TXA2,PGI2),amylase activity and the levels of Cr were researched ,The therapeutic efficiency of Ozagrel in SAP was observed. For analysis of test results, we used the SAS system by computer. Results: The levels of TNF-(,TXA2,PGI2 were all upregulation in SAP. GroupB versus GroupA :the difference of TNF-(,TXA2 were all of statistical significance(P(0.05). the difference of PGI2 was of statistical significance at 3 hour in plasma and all time points in pancreas, kidney. (P(0.05); GroupB versus Group C: the difference of PGI2 in pancreas has not the statistical significance at 3,6 and 12 hours(P(0.05), the difference of PGI2 in plasma has not the statistical significance at 6 hour and before death (P(0.05),the others (including TNF-(,TXA2,PGI2 ) was of statistical significance(P(0.05); Group B versus Group D : Weather in plasma or in tissue, the difference of TNF-(,TXA2,PGI2 has not the statistical significance at all time point (P(0.05). The obvious change of TNF-(,TXA2,PGI2 was positively correlated with the damage of kidney and pancreas.Conclusions: TNF-(,TXA2,PGI2 play an essential role to induce SAP and the kidney damage, Ozagrel could inhibit the production of TXA2 and alleviate the risk of pancreas and kidney damage. Ozagrel may be the efficient therapy to prevent the development of SAP and kidney damage... |
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