Portal-Endocrine and Gastric-Exocrine Drainage Technique in Pancreatic Transplantation

Background: Pancreas transplant (PTx) is an established treatment for patients with diabetes mellitus. Diagnosisof rejection has continued to be problematic. In 2007, a new technique of PTx with portal-endocrineand gastric exocrine (P-G) drainage was first performed at our institution. This technique facilitates accessto pancreas allograft.Objective: To report our experience with the first 30 patients who underwent PTx using P-G technique.Methods: The first 30 patients who underwent PTx between 2007 and 2009 were studied. In these patients,arterial and venous anastomosis was similar to standard portal-enteric (P-E) technique, thoughcontrary to other techniques of enteric drainage, the end of allograft jejunum was anastomosed to theanterior aspect of the stomach.Results: Donor and recipient demographic data, number of antigen matches and immunosuppressant werecollected. All patients achieved euglycemia. 3 patients underwent pancreatectomy: 2 due to vessel thrombosisand 1 due to chronic rejection. 3 patients died—2 with functioning pancreatic and renal allografts.7 patients with CMV and 4 patients with rejection were diagnosed with endoscopy of allograft duodenumand treated. 1-year patient and graft survival was 94% and 85%, respectively.Conclusion: This novel technique of PTx has proven to be safe with good patient and allograft survival. Accessto donor duodenum and pancreas allograft via endoscopy is unique to this technique and providesthe added advantage of life-long easy access to allograft

Effects of dextran and pentoxifylline on hemorrhagic shock-induced P-selectin expression

Background. Dextran and pentoxifylline have been shown to prevent leukocyte-endothelium adherence encountered after hemorrhagic shock, P-Selectin is the first endothelial cell adhesion molecule to be upregulated after an ischemic insult. We investigated the effects of resuscitation with dextran 70 and administration of pentoifylline during resuscitation on hemorrhagic shock-induced P-selectin expression

Kinetics of P-selectin expression in regional vascular beds after resuscitation of hemorrhagic shock: A clue to the mechanism of multiple system organ failure

Leukocyte-endothelial cell interactions play an important role in mediating organ dysfunctions observed after hemorrhagic shock. P-selectin is the first endothelial cell adhesion molecule to be upregulated after an ischemic insult. The objective of this study was to define kinetics of P-selectin expression in different regional vascular beds of mice exposed to hemorrhagic shock. In-vivo P-selectin expressions were determined using dual radiolabeled monoclonal antibody technique in lungs, heart, liver, kidneys, intestinal mesentery, stomach, small bowel, and colon 0.5, 1, 2, 5, 10, and 24 h after resuscitation of 40 mmHg hemorrhagic shock. In another group, P-selectin expression was determined in same organs 5 h after resuscitation of 30 mmHg hemorrhagic shock. Hemorrhagic shock of 40 mmHg caused significant upregulation of P-selectin in lungs and liver at 30 min after resuscitation (P < 0.001). There was a second and more pronounced upregulation of P-selectin in lungs and liver at 5 h after resuscitation (P < 0.001). In heart, intestinal mesentery, stomach, small bowel, and colon, P-selectin was not upregulated until 5 h after resuscitation from 40 mmHg hemorrhagic shock (P < 0.001). While hemorrhagic shock of 40 mmHg did not cause P-selectin upregulation in kidneys, hemorrhage to 30 mmHg did elicit a significant increase at 5 h after resuscitation (P < 0.001). We conclude that P-selectin is upregulated after resuscitation of hemorrhagic shock in lungs, liver, heart, stomach, and intestines. P-selectin upregulation in kidneys only takes place after more severe hemorrhagic shock

Role of superoxide in hemorrhagic shock-induced P-selectin expression

Superoxide has been implicated in the regulation of endothelial cell adhesion molecule expression and the subsequent initiation of leukocyte-endothelial cell adhesion in different experimental models of inflammation. The objective of this study was to assess the contribution of oxygen radicals to P-selectin expression in a murine model of whole body ischemia-reperfusion, i.e., hemorrhage-resuscitation (H/R), with the use of different strategies that interfere with either the production (allopurinol, CD11/CD18-deficient or p47(phox)-/- mice) or accumulation [intravenous superoxide dismutase (SOD), mutant mice that overexpress SOD] of oxygen radicals. P-selectin expression was quantified in different regional vascular beds by use of the dual-radiolabeled monoclonal antibody technique. H/R elicited a significant increase in P-selectin expression in all vascular beds. This response was blunted in SOD transgenic mice and in wild-type mice receiving either intravenous SOD or the xanthine oxidase inhibitor allopurinol. Mice genetically deficient in either a subunit of NADPH oxidase or the leukocyte adhesion molecule CD11/CD18 also exhibited a reduced P-selectin expression. These results implicate superoxide, derived from both xanthine oxidase and NADPH oxidase, as mediators of the increased P-selectin expression observed in different regional vascular beds exposed to hemorrhage and retransfusion