Preservation of cortical microcirculation after kidney ischemia-reperfusion: value of an iron chelator.
Treatment of suprarenal aneurysms and renal artery reconstructions are both responsible for normothermic ischemia of the kidney (during clamping) followed by reperfusion (declamping). During reflow through an organ undergoing ischemia the production of free radicals can be associated with cell injury and a no-reflow phenomenon characterized by perfusion defects after a period of transient hyperemia. The objectives of this study were to demonstrate the existence of this phenomenon in the kidney undergoing ischemia followed by reperfusion and to test the potential protection afforded by an iron chelator (desferrioxamine) since free radical reactions are catalyzed by iron. Adult New Zealand white rabbits were divided into the following three groups: group A, 15 minutes of ischemia plus 10 minutes of reperfusion; group B, 60 minutes of ischemia plus 10 minutes of reperfusion; and group C, 60 minutes of ischemia plus 10 minutes of reperfusion combined with infusion of desferrioxamine (50 mg/kg). Cortical microcirculation in the kidney was measured by laser Doppler flowmeter before ischemia and 1, 5, and 10 minutes after reperfusion. Vitamin E content was determined in the cortex of the left kidney after 10 minutes of reperfusion and compared with that of the right (control) kidney. After 1 minute of reperfusion the cortical microcirculatory flow was significantly increased in all three groups (reactive hyperemia). In groups A and C blood flow returned to preclamping values after 10 minutes of reperfusion; however, blood flow in group B remained significantly reduced (29.2% +/- 10.5%) after 5 minutes of reperfusion with a further reduction to 48.5% +/- 5.7% after 10 minutes. These findings were correlated with the dosage of vitamin E since the vitamin E content was greatly reduced by 46.7% +/- 7.8% in group B but did not change significantly in groups A and C. This study shows that 60 minutes of normothermic ischemia is followed by a significant reduction in cortical microcirculatory flow (no-reflow phenomenon). Infusion of an iron chelator (desferrioxamine), however, which decreases the intensity of lipid peroxidation induced by the free radicals, preserves the microcirculatory flow.
Defraigne
J O
JO
Service de Chirurgie Cardio-Vasculaire, Centre Hospitalo-Universitaire de Liège, Belgium.
Pincemail
J
J
Detry
O
O
Franssen
C
C
Meurisse
M
M
Limet
R
R
D000818:Animals; D003250:Constriction; D003676:Deferoxamine / Q000494:pharmacology / Q000627:therapeutic use*; D007511:Ischemia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology* / Q000517:prevention & control; D007672:Kidney Cortex / Q000098:blood supply*; D017078:Laser-Doppler Flowmetry; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology*; D008954:Models, Biological; D011817:Rabbits; D012079:Renal Circulation / Q000187:drug effects; D015424:Reperfusion; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology* / Q000517:prevention & control; D014810:Vitamin E / Q000378:metabolism
D014810:Vitamin E; D003676:Deferoxamine