Experimental Study On The Prevention Of Aggravation Of Acute Pancreatitis By Thoracic Epidural Anesthesia In Rats

Objective In this study, we established the rat model of acute aggravatingpancreatitis and intervened by the epidural block at the edema stage of model and thenobserved the changes of tumor necrosis factor-alpha (TNF-α), interleukin-6(IL-6),serum amylase (AMY) and acinar cell apoptosis circumstances, and aimed to explore theeffect of thoracic epidural anesthesia intervention on acute pancreatitis.Methods Healthy adult male SD rats were randomly divided into controlgroup(group C, n=8)，acute pancreatitis group（group AP，n=16），saline treatmentgroup(group NS，n=16), ropivacaine treatment group(TEA group, n=16)，and the lastthree groups again into12,24h two time points（12h，n=8；24h，n=8），AP animal modelswere made by intraperitoneal injecting of8%L-arginine （3×150mg/100g bm），eachonce interval for1hour. In group C, L-arginine was substituted for the same amount ofsaline at the same time.The24h time point rats were treated as follows at12thh aftermodeling：Ropivacaine（0.1%，0.01ml／100g bm） was infused（each infusion intervalfor2hours）via epidural anesthetic catheter in the TEA group and normal saline （0.01ml／100g bm）was infused instead of ropivacaine in the same way in the NS group，theAPgroup not treated. Each group of rats were collected blood before modeling （T0）and at12th（T1）,24thh（T2）after modeling and the12h time point rats were killed at T1, andthe remaining rats were sacrificed at T2. Observe intraperitoneal situation by the nakedeyes. Use automatic biochemical analyzer to detect the serum amylase(AMY). Adoptdouble-antibody sandwich ELISA to detect the serum levels of TNF-α and IL-6. HEstaining of pancreatic tissue to observation and pathological score under themicroscopeand. Use TUNEL to observe acinar cell apoptosis circumstances.Results⑴Blood serum biochemical index:①Compared with group C, thelevels of serum AMY、TNF-α and IL-6were significantly increased in the rest of threegroups（P<0.01）.②Compared with group AP and group NS, the levels of serum TNF-α and IL-6was significantly reduced in the TEA group at T2(P<0.05), and had nodifference at T1(P>0.05).③Comparison of T2and T1,the levels of serum AMY、TNF-α and IL-6were no statistically significant in the TEA group（P＞0.05）andsignificantly increased in the AP group and NS group. Comparison of T1and T0, thethree groups were significantly higher(P <0.01). No significant change in group C at alltime points.⑵The observation of pathology:①In the AP group, NS group and TEAgroup,pancreatic tissue was mainly manifested as interstitial edema, acinar swellingandand inflammatory cell infiltration at T1. At T2, the C group pancreatic tissue was clear; APgroup and NS group showed large areas of hemorrhage and necrosis and acinar lobularstructures destroyed, surrounded by a large number of inflammatory cell infiltration; TEAgroup cell necrosis was significantly reduced, less inflammatory cells②Compared withgroup C，the pathological scores were significantly higher in the rest of three groups (P<0.01). Compared with the AP and NS group，that of group TEA were significantly lower(P <0.05) at T2. Pancreatic tissue pathology score was positively correlated with TNF-αand IL-6（r=0.89, r=0.77，P<0.01）.⑶acinar cell apoptosis: AP group and NS groupobserved a small amount of apoptotic cells, little or no observed in group C, The TEAgroup has a large number of apoptotic cells.Conclusion⑴By the method of intraperitoneal injection of large doses of8%L-arginine（3×150mg/100g bm）, each injection interval of1hour, we successfullyconstructed the rats model of acute aggravating pancreatitis.⑵Inflammatory factorsand acinar cell apoptosis play an important role in the AP course.⑶Epidural anesthesiacan effectually mitigate aggravation of acute pancreatitis, and its possible mechanismsas follows: block incoming noxious stimuli, reduce the stress response, inhibit therelease of inflammatory mediators, thereby induce acinar cell apoptosis, improve theoutcome of the pancreas.