title: Gut ischemia/reperfusion induced acute lung injury is an alveolar macrophage dependent event.
abstract: BACKGROUND
  Although the role of the lung alveolar macrophage (AM) as a mediator of acute lung injury (ALI) after lung ischemia/reperfusion (I/R) has been suggested by animal experiments, it has not been determined whether AMs mediate ALI after intestinal I/R. The objective of this study was to determine the effect of AM elimination on ALI after intestinal I/R in rats.
  
  
  METHODS
  Male Wistar rats (n = 90) were randomly divided into three groups: the clodronate-liposomes (CLOD-LIP) group received intratracheal treatment with CLOD-LIP; the liposomes (LIP) group received intratracheal treatment with LIP; and the nontreated (UNTREAT) group received no treatment. Twenty-four hours later each group was randomly divided into three subgroups: the intestinal I/R subgroup was subjected to 45-minute intestinal ischemia and 2-hour reperfusion; the laparotomy (LAP) subgroup was subjected to LAP and sham procedures; the control (CTR) subgroup received no treatment. At the end of reperfusion, ALI was quantitated in all the animals by the Evans blue dye (EBD) method.
  
  
  RESULTS
  ALI values are expressed as EBD lung leakage (microg EBD/g dry lung weight). EBD lung leakage values in the CLOD-LIP group were 32.59 +/- 12.74 for I/R, 27.74 +/- 7.99 for LAP, and 33.52 +/- 10.17 for CTR. In the LIP group, lung leakage values were 58.02 +/- 18.04 for I/R, 31.90 +/- 8.72 for LAP, and 27.17 +/- 11.48 for CTR. In the UNTREAT group, lung leakage values were 55.60 +/- 10.96 for I/R, 35.99 +/- 6.89 for LAP, and 30.83 +/- 8.41 for CTR. Within each group, LAP values did not differ from CTR values. However, in the LIP and UNTREAT groups, values for both the LAP and CTR subgroups were lower than values for the I/R subgroup (p < 0.001). The CLOD-LIP I/R subgroup value was less (p < 0.001) than the I/R subgroup values in the LIP and UNTREAT groups. These results indicated that I/R provokes ALI that can be prevented by CLOD-LIP treatment, and further suggested that AMs are essential for ALI occurrence induced by intestinal I/R in rats.
authors.affiliation: Laboratory of Medical Investigation of the 3rd Division of Surgical Clinic, Hospital das Clinicas, University of Sao Paulo School of Medicine, Sao Paulo, Brazil.
authors.forename: Luciana Borsoi
authors.initials: LB
authors.lastname: Moraes
authors.forename: Abel Hiroshi F
authors.initials: AH
authors.lastname: Murakami
authors.forename: Belchor
authors.initials: B
authors.lastname: Fontes
authors.forename: Renato Sergio
authors.initials: RS
authors.lastname: Poggetti
authors.forename: Nico
authors.initials: N
authors.lastname: van Rooijen
authors.forename: Riad Nain
authors.initials: RN
authors.lastname: Younes
authors.forename: Ana Maria Cattani
authors.initials: AM
authors.lastname: Heimbecker
authors.forename: Dario
authors.initials: D
authors.lastname: Birolini
mesh_terms: D000818:Animals; D050071:Bone Density Conservation Agents / Q000008:administration & dosage*; D002199:Capillary Permeability; D004002:Clodronic Acid / Q000008:administration & dosage*; D007422:Intestines / Q000098:blood supply*; D008081:Liposomes; D016676:Macrophages, Alveolar / Q000187:drug effects* / Q000502:physiology; D008297:Male; D010587:Phagocytosis; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000150:complications*; D012128:Respiratory Distress Syndrome / Q000209:etiology* / Q000503:physiopathology
chemical_list: D050071:Bone Density Conservation Agents; D008081:Liposomes; D004002:Clodronic Acid