Objecltive To intensify the coordination and nursing in the operation room in order to prevent surgical site infection after gastrointestinal operation. Methods 337 medical history of patients received gastrointestinal operation and third rate healing from 1999 to 2006 were collected. A series of intensified measures were applied to surgical site infection from 2003 gradually, including invocation of new surgical handwashing method, modified skin disinfection manner, adoption of degreasing with ethanol first before disinfection with iodophor, placement of incision protector and clean bag for incision protection after entering abdomen, changing to use new gastrointestinal anastomofic thimerosal,standardization of operation order and clean manage-ment in operation room. The incidence rate of surgical site infection after gastrointestinal operation of patients from 1999 to 2002 and from 2003 to 2006 underwent χ2 test. Results The incidence rate of surgical site in-fection after gastrointestinal operation greatly decreased after adoption of intensified nursing intervention, Signifi-cant difference existed in rate of patients with third rate healing between the year 1999 to 2002 and 2003 to 2006. Conclusions Modified nursing intervention for surgical incision after gastrointestinal operation can de-crease incision infection rate evidently.

Objective To evaluate the changes of splanchnic hemodynamics after selective decongestive devascularization shunt of gustrosplenic region (SDDS-GSR) in the treatment of patients with portal hypertension. Methods All these 41 portal hypertensive patients underwent a combination surgery including partially occlusion of the splenic artery, Warren distal splenorenal shunt and devascularization. Postoperative patients were followed-up by ultrasonography for changes of splanchnic hemodynamics. Results were compared with that of 21 healthy volunteers. Results The thickness of spleen 2 weeks and 1 year after surgery (47±8) mm, (46±8) nun decreased from preoperative (60±9) mm (P<0.01). The diameter of portal vein (1.13±0.19) cm and splenic artery (0.49±0.08) cm 2 weeks after surgery decreased (P<0.05) and that of hepatic artery (0.40±0.07) cm increased (P<0.05). Patients' preoperative portal vein blood flow volume (1716±1262) ml/min and splenic artery (1269±570) ml/min were larger than that of normal group (P<0.05), while that of hepatic artery (321±126) ml/min was significantly less than that of normal group (P<0.05). The portal blood flow (649±294) ml/min and that of splenic artery (446±254) ml/min 2 weeks after surgery decreased significantly (P<0.01). The hepatic artery blood flow (612±295) ml/min increased significantly (P<0.01). When reevaluated at 1 year the hepatic artery blood flow (401±152) ml/min was not significantly different compared with that before surgery and that in normal group (P>0.05). Conclusions There are significant alterations in hepatic and splenic hemodynamics in patients with portal hypertension, and that SDDS-GSR can partially reverse the chaos of the hepatic and splenic hemodynamics in cirrhotic portal hypertensive patients.

Objective To explore the influence of different blood gas strategies on cerebral protection and blood gas analysis during moderate hypothermic cardiopulmonar.Methods Patients under cardiac valve replacement with extracorporeal circulation (ECC) were performed in this study.The cerebral blood flow (CBF) and regional cerebral oxygen saturation (rSO2) were monitored at 5 points:(1)Induction of anesthesia (T1),(2) after 10 min of the beginning of cardiopulmonary bypass (T2),(3) during the moderate hypothermic phase of CBP managed by the alpha-stat after calibrate blood gas 15 min (T3),(4) pH-stat followed,after calibrate blood gas 15 min (T4),and (5) 10 min after CBP (T5).pH and pCO2 in patients were recorded and analyzed at T3 and T4.Results The CBF of T2 and T3 was lower than that of T1,but the difference was not significant (t =2.841,2.711;P =0.062,0.080).The CBF of T4 and T5 was higher than that of T3,but the difference was not significant (t =1.793,2.135;P =0.119,0.066).The CBF of T5 resumed to before operation.The rSO2 of T2 and T3 was lower than that of T1,but the difference was not significant (t =1.821,2.032;P =0.132,0.267),the rSO2 ofT4 and T5 was higher than that ofT3,but the difference was not significant (t =1.879,2.021;P =0.312,0.075).The rSO2 of T5 resumed to before operation.However,the pH was much lower in pH-stat than alpha-stat (t =17.541,P =0.000) and the pCO2 was much higher than alpha-stat (t =13.914,P =0.000).Conclusions Both pH-stat and alpha-stat have cerebral protection effects.However,compared to pH-stat,alpha-stat could reduce the possibility of acidosis,and maintain the acid-base equilibrium.

A stable and reliable infected necrotizing pancreatitis (INP) model in rats was established in order to study the pathophysiological mechanism and pathological development rule of INP and explore the new therapeutic methods for the diseases. Forty-six SD rats were randomly divided into 5 groups. The animals in group A received the injection of 5% sodium taurocholate into the pancreatic duct and those in group B underwent that of E. coli into the pancreatic duct. The rats in groups C, D and E were subjected to the injection of 5% sodium taurocholate in combination with different concentrations of E. coli (10(3), 10(4), 10(5)/mL, respectively) into the pancreatic duct. The dose of injection was 0.1 mL/100 g and the velocity of injection was 0.2 mL/min in all the 5 groups. Eight h after the injection, the survival rate of animals was recorded and the surviving rats were killed to determine the serum content of amylase and perform pathological examination and germ cultivation of the pancreatic tissue. The results showed that acute necrotizing pancreatitis model was induced by injection of 5% sodium taurocholate into the pancreatic duct. The positive rate of germ cultivation in group A was 12.5%. The acute necrotizing pancreatitis model was not induced by injection of E. coli into the pancreatic duct and the positive rate of germ cultivation in group B was 0. The INP model was established in groups C to E. The positive rate of germ cultivation was 60%, 100% and 100% and 8-h survival rate 100%, 100% and 70% in groups C, D and E, respectively. It was concluded that a stable and reliable model of INP was established by injection of 5% sodium taurocholate in combination with 10(4)/mL E. coli into the pancreatic duct with a dose of 0.1 mL/100 g and a velocity of 0.2 mL/min. The pathogenesis of INP might be that the hemorrhage and necrosis of pancreatic tissue induced by sodium taurocholate results in weakness of pancreatic tissue in fighting against the germs. Meanwhile, the necrotic pancreatic tissue provides a good proliferative environment for the germs.
Cholagogues and Choleretics/*pharmacology ; Disease Models, Animal ; Escherichia coli/*metabolism ; Injections, Intraperitoneal ; Pancreas/enzymology ; Pancreas/microbiology ; Pancreatic Ducts/enzymology ; Pancreatic Ducts/microbiology ; Pancreatitis, Acute Necrotizing/*chemically induced ; Pancreatitis, Acute Necrotizing/*microbiology ; Rats, Sprague-Dawley ; Taurocholic Acid/*pharmacology ; Time Factors

A stable and reliable infected necrotizing pancreatitis (INP) model in rats was established in order to study the pathophysiological mechanism and pathological development rule of INP and explore the new therapeutic methods for the diseases. Forty-six SD rats were randomly divided into 5 groups. The animals in group A received the injection of 5% sodium taurocholate into the pancreatic duct and those in group B underwent that of E. Coli into the pancreatic duct. The rats in groups C, D and E were subjected to the injection of 5% sodium tanrocholate in combination with different con-centrations of E. Coli (103, 104, 105/mL, respectively) into the pancreatic duct. The dose of injection was 0.1 mL/100 g and the velocity of injection was 0.2 mL/min in all the 5 groups. Eight h after the injection, the survival rate of animals was recorded and the surviving rats were killed to determine the serum content of amylase and perform pathological examination and germ cultivation of the pancre-atic tissue. The results showed that acute necrotizing panereatitis model was induced by injection of 5% sodium taurocholate into the pancreatic duct. The positive rate of germ cultivation in group A was 12.5%. The acute necrotizing pancreatitis model was not induced by injection of E. Coli into the pan-creatic duct and the positive rate of germ cultivation in group B was 0. The INP model was estab-lished in groups C to E. The positive rate of germ cultivation was 60%, 100% and 100% and 8-h sur-vival rate 100%, 100% and 70% in groups C, D and E, respectively. It was concluded that a stable and reliable model of INP was established by injection of 5% sodium taurocholate in combination with 104/mL E. Coli into the pancreatic duct with a dose of 0.1 mL/100 g and a velocity of 0.2 mL/min. The pathogenesis of INP might he that the hemorrhage and necrosis of pancreatic tissue in-duced by sodium taurocholate results in weakness of pancreatic tissue in fighting against the germs.Meanwhile, the necrotic pancreatic tissue provides a good proliferative environment for the germs.