Oxidative Insult Associated With Hyperoxic Cardiopulmonary Bypass in the Infantile Heart and Lung

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概要

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• Cardiopulmonary bypass(CPB)per se alters many factors simultaneously, in cluding free radical generation, which suggests that conventional hyperoxic CPB may produce oxidative injury in the infantile heart and lung. This study tests the hypothesis that CPB provokes oxidative cardiopulmonary changes and pulmonary endothelial dysfunction in immature piglets that can be prevented by free radical scavengers. We studied 15 2- to 3-week-old piglets. Five served as a control without CPB. Ten piglets underwent 60 min of CPB with a membrane oxygenator(Sarns). In 5 of these 10, the bypass prime was supplemented with N-mercaptopropionylglycine(MPG : 80 mg/kg)plus catalase(50, 000 U/kg), whereas the others were not treated. Pre- and post-bypass cardiopulmonary function was measured in terms of left ventricular end-systolic elastance [Ees] by a conductance catheter, the arterial / alveolar pO_2 ratio(a/A ratio)and static lung compliance. Conjugated dienes(A233 nm/mg lipid)were measured to detect lipid peroxidation in heart and lung tissue, and myocardial antioxidant reserve capacity [malondialdehyde(MDA)production in cardiac tissue incubated with the oxidant t-butyl hydroperoxide(t-BHP)] was assessed to detect oxidative changes. Pulmonary vascular resistance(PVR)and transpulmonary nitric oxide(NO)production were measured to assess pulmonary endothelial injury. Myocardial antioxdant reserve capacity was significantly reduced after 60 min of CPB, compared to control animals(MDA 779±100 vs 470±30 nmol/g protein, p<0.05 at t-BHP 2.0 mmol/L), without evidence of lipid peroxidation or myocardial dysfunction. Pulmonary vascular resistance after CPB was dramatically increased(83±12 to 212±30, p<0.05)without any change in lung function. In parallel to pulmonary vasoconstriction, NO production was significantly decreased after CPB(from 8.8±1.4 to 2.5±0.5 mmol/min/kg, p<0.05). The addition of antioxidants(MPG+catalase)to the prime significantly improved myocardial antioxidant status(MDA : 604±30 vs 779±100 nmol/g protein, p<0.05)and pulmonary vascular resistance(114±29 vs 212±30, p<0.05 vs no-treatment group). In conclusion, the present study confirms that 1)Cardiopulmonary bypass produces substantial oxidative stress in normal immature myocardium, as assessed by reduced antioxidant reserve capacity ; 2)CPB impairs pulmonary endothelial function, characterized by NO production, resulting in pulmonary vasoconstriction ; and 3)These deleterious effects can be prevented by the addition of antioxidants(MPG/catalase)to the pump prime.

• 社団法人日本循環器学会の論文
• 1996-05-20

著者

• Buckberg Gerald

  Department Of Cardiothoracic Surgery Ucla School Of Medicine

• Morita Kiyozo

  Department Of Cardiac Surgery Jikei University School Of Medicine

• Morita Kiyozo

  Department Of Cardiovascular Surgery Jikei University School Of Medicine

• Ihnken Kai

  Department of Cardiothoracic Surgery, UCLA School of Medicine

• Ignarro Louis

  Department of Pharmacology, UCLA School of Medicine

• Ihnken Kai

  Department Of Cardiothoracic Surgery Ucla School Of Medicine

• Ignarro Louis

  Department Of Molecular And Medical Pharmacology University Of California At Los Angeles

• Ignarro Louis

  Department Of Pharmacology Ucla School Of Medicine

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