title: Accumulation of platelets in rat syngeneic lung transplants: a potential factor responsible for preservation-reperfusion injury.
abstract: BACKGROUND
  Platelets are known to play an important role in the pathogenesis of adult respiratory distress syndrome as well as preservation-reperfusion injury of liver allografts. However, the role of platelets in pulmonary preservation-reperfusion injury is unknown. In this study, we examined whether the extent of platelet accumulation in the preserved and subsequently reperfused lungs correlated with the degree of preservation-reperfusion injury in a rat lung isotransplant model.
  
  
  METHODS
  Heart-lung blocks from donor rats were flushed with and preserved in modified Euro-Collins solution at 4 degrees C for 0 hr (n=5), 6 hr (n=6), and 24 hr (n=6). The left lung was divided from the heart-lung block, transplanted into the recipient rat, and reperfused for 1 hr. Lung injury was evaluated by the left-to-right pulmonary blood flow ratio, the weight gain of the isograft, and the scores for histological categories of lung injury (intra-alveolar edema, intra-alveolar hemorrhage, and capillary congestion). Small portions of the lung isograft were excised and stained with an antibody specific for rat platelets. A scoring system was developed to semiquantitate the intensity of antibody staining in isografts.
  
  
  RESULTS
  Lung isografts were injured and platelets accumulated in the capillaries in proportion to the length of preservation endured before transplantation. The extent of platelet accumulation evaluated by our morphological scoring system correlated significantly with the degree of lung injury assessed by the blood flow ratio (P<0.001), the weight gain (P<0.001), and the histological scores for intra-alveolar hemorrhage (P<0.05) and for capillary congestion (P<0.001).
  
  
  CONCLUSIONS
  The results of this study suggest that platelet accumulation is a potential factor responsible for preservation-reperfusion injury of lung isografts in the rat.
authors.affiliation: Department of Cardiothoracic Surgery, The Cedars-Sinai Medical Center Burns and Allen Research Institute, UCLA School of Medicine, Los Angeles, California 90048, USA.
authors.forename: Y
authors.initials: Y
authors.lastname: Okada
authors.forename: A M
authors.initials: AM
authors.lastname: Marchevsky
authors.forename: X J
authors.initials: XJ
authors.lastname: Zuo
authors.forename: J A
authors.initials: JA
authors.lastname: Pass
authors.forename: R M
authors.initials: RM
authors.lastname: Kass
authors.forename: J M
authors.initials: JM
authors.lastname: Matloff
authors.forename: S C
authors.initials: SC
authors.lastname: Jordan
mesh_terms: D000818:Animals; D000906:Antibodies; D001792:Blood Platelets / Q000473:pathology / Q000502:physiology*; D002196:Capillaries; D019085:Fluorescent Antibody Technique, Direct; D006321:Heart; D006982:Hypertonic Solutions; D008168:Lung; D016040:Lung Transplantation / Q000473:pathology* / Q000502:physiology*; D008297:Male; D009926:Organ Preservation; D051381:Rats; D011917:Rats, Inbred Lew; D012044:Regression Analysis; D013997:Time Factors; D014185:Transplantation, Isogeneic
chemical_list: D000906:Antibodies; C037096:Euro-Collins' solution; D006982:Hypertonic Solutions