Small bowel graft function and structure after allo- and xeno-transplantation.
Department of Surgery, Sapporo Medical University, Japan.Transplantation Proceedings (Impact Factor: 0.95). 11/1996; 28(5):2582-4.
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ABSTRACT: The study was designed to evaluate the role of neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) in ischemia-reperfusion injury (IRI) and acute rejection (AR) in rat intestinal transplantation, by administration of nitric oxide inhibitor N(G)-nitro-L-arginine methyl ester (LNAME). Rats that underwent orthotopic intestinal transplantation were assigned to 2 sets of groups: (1) iso-geneic group (Lewis-Lewis), L-NAME 0 mg/kg/d group (1-1), 4 mg/kg/d (group 1-2), or 8 mg/kg/d (group 1-3) injected intraperitoneally or (2) allogeneic group (Dark Agouti-Lewis), L-NAME 0 mg/kg/d (group 2-1) or 8 mg/kg/d (group 2-2) injected intraperitoneally. We examined survival times, light microscopy as well as maltose absorption tests. The nNOS and iNOS activities were measured by immunohistochemical methods. Histologic examination showed inhibited iNOS activity compared with group l-l, and Park scores decreased significantly in group 1-2 at 30 minutes after reperfusion (1.42 ± 0.38 vs 2.58 ± 0.49, P < .01). Both iNOS and nNOS activities were inhibited and Park scores increased significantly in group 1-3 from 30 minutes to day 3 after reperfusion (P < .0l). nNOS activity decreased and iNOS activity increased among group 2-1 during AR. Compared with group 2-1, iNOS activity was inhibited, progression of AR delayed, and survival significantly prolonged in group 2-2 (10.17 ± 0.98 vs 6.83 ± 0.75, P < .01). This study suggested that decreased nNOS and increased iNOS activity both contributed to IRI and AR. More importantly, nNOS more importantly than iNOS activity was closely related to graft structure and function.Transplantation Proceedings 07/2013; 45(6):2497-501. DOI:10.1016/j.transproceed.2013.04.008 · 0.95 Impact Factor
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ABSTRACT: This study was designed to evaluate the role of nitric oxide (NO) in ischemia-reperfusion injury (IRI) and acute rejection (AR) in rat intestinal transplantation, using administration of the NO inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). Rats that underwent orthotopic allogeneic intestinal transplantation were assigned to 2 groups. In the normal allograft group (Wistar to Sprague-Dawley rats), L-NAME 0 mg/kg/d (group 1-1), 4 mg/kg/d (group 1-2), 8 mg/kg/d (group 1-3), or 12 mg/kg/d (group 1-4) was injected intraperitoneally. In the high responder allograft group (Dark Agouti to Lewis rats), L-NAME 0 mg/kg/d (group 2-1) or 8 mg/kg/d (group 2-2) was injected intraperitoneally. Survival times were observed and maltose absorption tests performed as well as light microscopic examination of the grafts. The mean survival time of group 1-3 was significantly prolonged compared with group 1-1 (P < .01). In group 2, the survival time of group 2-2 was significantly prolonged compared with group 2-1 (P < .01). Histological changes showed IRI was attenuated in group 1-2 compared with group 1-1, whereas it was aggravated in groups 1-3 and 1-4. Treatment with L-NAME (8 mg/kg/d) attenuated the graft damage of AR in groups 1 and 2. Maltose absorption tests showed that inhibition of NO impaired maltose absorption. This study suggested that NO plays a dual role as both a cytotoxic and a cytoprotective factor in IRI, and may serve as a kind of cytotoxic medium in AR in rat intestinal allotransplantation.Transplantation Proceedings 12/2008; 40(10):3342-5. DOI:10.1016/j.transproceed.2008.03.167 · 0.95 Impact Factor
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