title: Roles of neuronal nitric oxide synthase and inducible nitric oxide synthase in intestinal transplantation of rats.
abstract: OBJECTIVE
  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).
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors: Department of Gastrointestinal Surgery, Second Affiliated Hospital, Harbin Medical University, Harbin, China.
authors: X L
authors: XL
authors: Li
authors: X M
authors: XM
authors: Zou
authors: G
authors: G
authors: Nie
authors: M L
authors: ML
authors: Song
authors: G
authors: G
authors: Li
mesh_terms: D000818:Animals; D015536:Down-Regulation; D004791:Enzyme Inhibitors / Q000008:administration & dosage; D005260:Female; D006084:Graft Rejection / Q000201:enzymology* / Q000209:etiology / Q000473:pathology / Q000517:prevention & control; D006085:Graft Survival / Q000187:drug effects; D007274:Injections, Intraperitoneal; D007408:Intestinal Absorption; D007422:Intestines / Q000098:blood supply / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology / Q000637:transplantation*; D008297:Male; D008320:Maltose / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000008:administration & dosage; D052248:Nitric Oxide Synthase Type I / Q000037:antagonists & inhibitors / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051381:Rats; D011917:Rats, Inbred Lew; D015427:Reperfusion Injury / Q000201:enzymology* / Q000209:etiology / Q000473:pathology / Q000517:prevention & control; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D004791:Enzyme Inhibitors; D008320:Maltose; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; C496322:Nos1 protein, rat; C496318:Nos2 protein, rat; D019331:NG-Nitroarginine Methyl Ester