Background: The suppressed production of nitric oxide (NO), associated with endothelial dysfunction, is thought to be a cause of ischemia and reperfusion injury of the liver. But findings of the salutary effects of NO enhancement on such injury have been conflicting. In this study, we tested our hypothesis that NO enhancement would attenuate ischemic liver injury. For this purpose, an NO precursor, L-arginine, and a novel NO donor, FK409, were applied to a 2-hour total hepatic vascular exclusion model in dogs.

A case of massive intestinal blood loss from multiple duodeno-jejunal diverticula is described. A 39-year-old man was referred to our hospital because of recurrent bloody stool and worsening anemia. Upper and lower endoscopy, selective abdominal angiography, and radionuclide scanning were performed to seek the cause of the intestinal bleeding, but none of these studies revealed the source of bleeding. Small-bowel barium follow-through examination showed numerous diverticula in the distal duodenum and proximal jejunum. Excision of the duodenal diverticulum and resection of the involved portion of the jejunum cured the patient. On histopathological examination, an ulcerative lesion with an exposed vessel suggestive of the source of bleeding was seen in the resected duodenal diverticulum. Although duodeno-jejunal diverticula are rare, the importance of a careful search for this malformation in a patient with intestinal blood loss is stressed.

LAZAROIDS, 21-aminosteroids lacking steroid activity have cytoprotective properties against iron-dependent lipid peroxidation. 1 In addition to their antioxidant properties, lazaroids exert their cytoprotective effect by inhibiting arachidonic acid release, membrane stabilization, suppression of Kuppfer cell activation, and down-regulation of cytokine expression and release. 1-3 While previous reports have shown that lazaroids are effective in reducing ischemia and reperfusion injury to many different organ systems, there have been conflicting reports of the potency of the various lazaroid compounds. 4 In this study, we examined the potency and effectiveness of the three major lazaroid compounds in protecting organs against ischemia and reperfusion injury. RESULTS Except for Group A1, the lazaroid infusion was well tolerated. Infusion of lazaroid A1 (high dose) was associated with arrhythmia and hypotension. Two-week animal survival in the control group (30%) was significantly worse than the treated groups (all but one treated

Hepatic grafts from non-heartbeating donors may alleviate the organ shortage, but they inherently suffer from warm ischemia. In the present study, we tested our hypothesis that augmentation of endogenous adenosine by inhibition of nucleoside transport with R75231 attenuates ischemic liver injury. Adult female beagle dogs underwent 2-hr hepatic vascular exclusion with venovenous bypass. R75231 was given to the animals by continuous intravenous infusion for 30 min before ischemia at a dose of 0.1 mg/kg (Group 2, n=6), 0.05 mg/kg (Group 3, n=6), or 0.025 mg/kg (Group 4, n=6). Nontreated animals were used as the control (Group 1, n= 10). Animal survival, hepatic tissue blood flow, liver function, and histopathology were analyzed. Two-week animal survival was 30% in Group 1, 83% in Group 2, 100% in Group 3, and 100% in Group 4. Postreperfusion hepatic tissue blood flow was markedly improved by the treatment. Treatment significantly attenuated liver enzyme release, lipid peroxidation, and changes in adenine nucleotides and purine catabolites. Structural abnormality of the liver after reperfusion was markedly improved by R75231 treatment, showing better architecture and less neutrophil infiltration. Preischemic administration of a nucleoside transport inhibitor ameliorated ischemic liver injury due to the positive effects of augmented endogenous adenosine, and is applicable clinically when the liver is procured from a controlled non-heartbeating donor.

horacoabdominal aortic aneurysm (TAAA) is not considered on indication for endovascular stent-graft repair because of the need to revascularize the visceral vessels. This article details for the first time a case of TAAA repair in which an endovascular stent graft was placed after reconstruction of the visceral vessels.