Surgical management for chronic pancreatitis.

This study reviewed the results of surgery for chronic pancreatitis. We also attempted to identify any factors that may influence outcome. A 10-year retrospective chart review was carried out on all patients undergoing surgery for the diagnosis of chronic pancreatitis. Twenty-three patients were identified. Alcohol was the most common etiology, but other causes were identified. All but two patients had abnormal ductal anatomy on endoscopic retrograde cholangiopancreatography. A total of 23 patients underwent six different operations. There were five complications and no perioperative deaths. Only one patient had to be readmitted for pancreatitis during follow-up. The majority of patients reported some improvement with their pain. Patients who continued to use alcohol had the worst results in regard to weight gain and pain control. The results of our study are consistent with the current literature in regard to morbidity and mortality. Surgical treatment had minimal effect on endocrine and exocrine function. Weight loss was avoided in the majority of patients. Addition of biliary bypass to the Puestow procedure did not increase morbidity. Poorest results were obtained in patients who continued to use alcohol. A basic algorithm for management of this disease process is given.

Both ischemic and pharmacological preconditioning decrease hepatic leukocyte/endothelial cell interactions.

BACKGROUND: Ischemic preconditioning has been shown to protect some tissues from ischemia/reperfusion (I/R) injury. Adenosine is believed to play an important role by attenuating leukocyte-endothelial cell adhesive interactions. Dipyridamole increases adenosine bioavailability. The purpose of this study was to evaluate the effects of mechanical (MPC) and pharmacological preconditioning (PPC) on leukocyte endothelial cell interaction in hepatic I/R injury. METHODS: C57BL6 mice were subjected to 30 min of ischemia to the left lobe of the liver. Groups tested at 30 min, 2, 5, 12, and 24 hr of reperfusion had 1) sham laparotomy (n = 10, 2) I/R (n = 25), 3) ischemic preconditioning with 5 min of ischemia and 10 min reperfusion before I/R (n = 25), and 4) (PPC) with dipyridamole (n = 25). Intravital microscopic examination was used to assess leukocyte/endothelial cell adhesion. Blood was drawn for leukocyte counts and liver function tests. RESULTS: A significant decrease in leukocyte rolling was observed at 30-min and 5-hr reperfusion intervals in the PPC and ischemic preconditioning groups compared with the I/R group. A significant decrease in leukocyte saltation was also observed in the PPC and MPC groups at 2, 5, and 12 hr of reperfusion when compared with the I/R group. aspartate aminotransferase was significantly decreased in the 5-hr preconditioning groups. There was not a significant decrease in the white blood cell count because of PPC or MPC vs. I/R CONCLUSIONS: Preconditioning decreases endothelial/ leukocyte interaction and reduces liver damage as measured by aspartate aminotransferase. These data prove that IPC and PPC provide some degree of hepatic protection in I/R injury.

Persantine attenuates hemorrhagic shock-induced P-selectin expression.

Ischemia/reperfusion (I/R), a phenomenon that is associated with conditions such as organ transplantation, trauma, vascular disease, and stroke, involves the recruitment of activated and adherent leukocytes that subsequently mediate tissue injury. Endothelial cell adhesion molecules such as P-selectin mediate I/R-induced leukocyte recruitment and allow the adherent leukocytes to damage the vascular wall and parenchymal cells. This study examines the influence of dypiridamole (persantine) on hemorrhagic shock (H/S)-induced P-selectin expression. H/S was induced in C57BL/6 mice by withdrawing blood to drop the mean arterial blood pressure to 30 to 35 mm Hg for 45 minutes. The mice were resuscitated by infusing the shed blood and Ringer's lactate (50% shed blood volume). In vivo P-selectin expression was determined using a dual monoclonal antibody technique in the heart, lung, liver, kidneys, stomach, small bowel, and colon of a control group, a hemorrhagic shock group, and a hemorrhagic shock group that was pretreated with Persantine (Boehringer, Ingelheim, Ingelheim, Germany). H/S significantly (P < 0.01) increased P-selectin expression in all regional vascular beds of untreated mice. Persantine treatment largely prevented the H/S-induced P-selectin expression in the same vascular beds. Persantine significantly attenuates the upregulation of P-selectin in the hemorrhagic shock model.