title: Pharmacologically induced ischemia-reperfusion syndrome in the rat small intestine.
abstract: BACKGROUND
  Reports of ischemia-reperfusion (I/R) injury in vivo describe experiments in which lesions are induced by the physical procedure of clamping, (I/RIC). We compare this procedure with a pharmacologic technique in which I/R injury is induced by drug superfusion (I/RID).
  
  
  METHODS
  We used rat intestine to determine whether the responses provoked by I/RIC, such as changes in reactive oxygen species (ROS) and nitric oxide levels, are also provoked by I/RID. To this end, rats were treated with allopurinol, SOD, catalase, L-NAME, and L-arginine. In both I/R models ischemia was maintained for 60 min, followed by 30 min of reperfusion.
  
  
  RESULTS
  In both ischemia models, we observed significant differences in Evans blue (vascular permeability) and LDH (tissue injury) concentrations during the reperfusion period compared with the control group. I/RIC always induced greater injury. However, proportionally, the degree of protection was similar in the two models for the different treatments assayed. This indicates that the pathophysiologic mechanisms are the same.
  
  
  CONCLUSIONS
  Our I/RID model induces a significant intestinal alteration during the reperfusion period and, also in general terms, this alteration is prevented or worsened in a similar and proportional way to that observed when using the classic I/RIC model. The I/RID model helps to explain the development and evolution of pathologies characterized by the induction of intermittent vasospasms that produce transitory reductions in vascular perfusion, which in turn can generate ROS though an I/R mechanism.
authors.affiliation: Unitat de Farmacología, Facultat de Medicina, Institut d'Investigacions Biomédiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain.
authors.forename: J
authors.initials: J
authors.lastname: Giménez-Crouseilles
authors.forename: P
authors.initials: P
authors.lastname: Puig-Parellada
mesh_terms: D000493:Allopurinol / Q000009:adverse effects*; D000818:Animals; D001120:Arginine / Q000009:adverse effects*; D002374:Catalase / Q000009:adverse effects*; D003250:Constriction; D007421:Intestine, Small / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D008297:Male; D023421:Models, Animal; D019331:NG-Nitroarginine Methyl Ester / Q000009:adverse effects*; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D013482:Superoxide Dismutase / Q000009:adverse effects*; D013997:Time Factors
chemical_list: D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D000493:Allopurinol; D001120:Arginine; D002374:Catalase; D013482:Superoxide Dismutase; D019331:NG-Nitroarginine Methyl Ester