title: Reperfusion of ischemic corporal tissue: physiologic and biochemical changes in an animal model of ischemic priapism.
abstract: OBJECTIVE
  To assess the physiologic and biochemical changes resulting from ischemia and reperfusion. Effective therapy for ischemic priapism reestablishes corporal venous outflow and arterial inflow and results in increased corporal partial pressure of oxygen. Data are limited concerning reperfusion injury of ischemic erectile tissue associated with reactive oxygen species (ROS) and the potential role of ROS scavengers in the clinical therapy of ischemic priapism.
  
  
  METHODS
  Anesthetized adult New Zealand white male rabbits (n = 7) were exposed to a low oxygen tension breathing gas to achieve hypoxia within the corpora cavernosa. This resulted in a mean systemic oxygen saturation of 60%. The pelvic nerve was electrically stimulated to induce penile erection, and the base of the erect penis was clamped. After varying durations of ischemia, the clamp was removed to allow reperfusion. We determined the intracavernosal oxygen tension, histologic changes, myeloperoxidase activity, and lipid peroxidation.
  
  
  RESULTS
  Corporal partial pressure of oxygen progressively decreased as the duration of priapism increased. A statistically significant increase was noted in myeloperoxidase activity and lipid peroxidation with corporal reperfusion. Polymorphonuclear leukocyte infiltration was documented in the ischemic reperfused tissue.
  
  
  CONCLUSIONS
  In the management of ischemic priapism, reperfusion causes erectile tissue injury owing to the presence of ROS. There is a need to investigate the utility of ROS scavengers and antioxidants in the management of ischemic priapism.
authors.affiliation: Department of Urology, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
authors.forename: Ricardo
authors.initials: R
authors.lastname: Munarriz
authors.forename: Kwangsung
authors.initials: K
authors.lastname: Park
authors.forename: Yue-Hua
authors.initials: YH
authors.lastname: Huang
authors.forename: Iñigo
authors.initials: I
authors.lastname: Saenz de Tejada
authors.forename: Robert B
authors.initials: RB
authors.lastname: Moreland
authors.forename: Irwin
authors.initials: I
authors.lastname: Goldstein
authors.forename: Abdulmaged M
authors.initials: AM
authors.lastname: Traish
mesh_terms: D000818:Animals; D002634:Chemotaxis, Leukocyte; D000860:Hypoxia / Q000150:complications; D007511:Ischemia / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D015227:Lipid Peroxidation; D008297:Male; D023421:Models, Animal; D009504:Neutrophils / Q000201:enzymology / Q000502:physiology; D018384:Oxidative Stress; D010413:Penis / Q000098:blood supply*; D009195:Peroxidase / Q000032:analysis; D011317:Priapism / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D011817:Rabbits; D017382:Reactive Oxygen Species; D015427:Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D017382:Reactive Oxygen Species; D009195:Peroxidase