title: Hyperbaric oxygen therapy induces kidney protection in an ischemia/reperfusion model in rats.
abstract: Ischemia/reperfusion (I/R) injury remains a major cause of graft dysfunction, which impacts short- and long-term follow-up. Hyperbaric oxygen therapy (HBO), through plasma oxygen transport, has been currently used as an alternative treatment for ischemic tissues. The aim of this study was to analyze the effects of HBO on kidney I/R injury model in rats, in reducing the harmful effect of I/R. The renal I/R model was obtained by occluding bilateral renal pedicles with nontraumatic vascular clamps for 45 minutes, followed by 48 hours of reperfusion. HBO therapy was delivered an hypebaric chamber (2.5 atmospheres absolute). Animals underwent two sessions of 60 minutes each at 6 hours and 20 hours after initiation of reperfusion. Male Wistar rats (n = 38) were randomized into four groups: sham, sham operated rats; Sham+HBO, sham operated rats exposed to HBO; I/R, animals submitted to I/R; and I/R+HBO, I/R rats exposed to HBO. Blood, urine, and kidney tissue were collected for biochemical, histologic, and immunohistochemical analyses. The histopathological evaluation of the ischemic injury used a grading scale of 0 to 4. HBO attenuated renal dysfunction after ischemia characterized by a significant decrease in blood urea nitrogen (BUN), serum creatinine, and proteinuria in the I/R+HBO group compared with I/R alone. In parallel, tubular function was improved resulting in significantly lower fractional excretions of sodium and potassium. Kidney sections from the I/R plus HBO group showed significantly lower acute kidney injury scores compared with the I/R group. HBO treatment significantly diminished proliferative activity in I/R (P < .05). There was no significant difference in macrophage infiltration or hemoxygenase-1 expression. In conclusion, HBO attenuated renal dysfunction in a kidney I/R injury model with a decrease in BUN, serum creatinine, proteinuria, and fractional excretion of sodium and potassium, associated with reduced histological damage.
authors.affiliation: Laboratory of Cellular, Genetic, and Molecular Nephrology, Faculty of Medicine, University of São Paulo, São Paulo, Brazil.
authors.forename: R J
authors.initials: RJ
authors.lastname: Ramalho
authors.forename: P S T
authors.initials: PS
authors.lastname: de Oliveira
authors.forename: R C
authors.initials: RC
authors.lastname: Cavaglieri
authors.forename: C
authors.initials: C
authors.lastname: Silva
authors.forename: P R B
authors.initials: PR
authors.lastname: Medeiros
authors.forename: D Martini
authors.initials: DM
authors.lastname: Filho
authors.forename: L F
authors.initials: LF
authors.lastname: Poli-de-Figueiredo
authors.forename: I L
authors.initials: IL
authors.lastname: Noronha
mesh_terms: D058186:Acute Kidney Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D006931:Hyperbaric Oxygenation; D007150:Immunohistochemistry; D007668:Kidney / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D011188:Potassium / Q000652:urine; D011507:Proteinuria / Q000209:etiology / Q000517:prevention & control; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D012964:Sodium / Q000652:urine; D013997:Time Factors
chemical_list: D015415:Biomarkers; D012964:Sodium; D003404:Creatinine; D011188:Potassium