Biphasic Elevation of Bilirubin Oxidation During Myocardial Ischemia Reperfusion

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Background The time course of oxidative stress involving nitric oxide (NO) after myocardial ischemia reperfusion (MIR) has not been elucidated in detail, so the present study was designed to assess the dynamics of oxidative stress after MIR, urinary excretion of oxidized bilirubin metabolites (ie, biopyrrins) and their generation in various organs. Methods and Results Rat models of MIR were created by occluding the left coronary artery for 30min followed by 48h of reperfusion. Levels of urinary biopyrrins increased biphasically at 8h and 24h after MIR. Biopyrrins were upregulated in the lungs at 8h after MIR, according to immunohistochemistry and ELISA, and at 24h biopyrrin expression was increased in the heart and lungs. The NO synthase inhibitor, N^G-monomethyl-Larginine, significantly diminished biopyrrin synthesis in the heart and lungs at 24h, but not in the lungs at 8h after MIR. Hemodynamic assessment revealed increased left ventricle end-diastolic pressure, suggesting that lung congestion influences pulmonary biopyrrin formation. Conclusions The dynamics of urinary biopyrrins might reflect earlier biopyrrin generation in the lungs and delayed formation in both the lungs and heart when NO is involved. Therefore, urinary biopyrrins can serve as a useful marker of systemic oxidative stress after MIR.
社団法人日本循環器学会の論文
2008-08-20