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CLINICAL STUDIES

Production of oxidative products of nitric oxide in infarcted human heart

^a Department of Experimental Cardiology, Huntington Medical Research Institutes, Pasadena, California, USA
^* Third Department of Internal Medicine, Showa University, School of Medicine, Tokyo, Japan

Manuscript received July 25, 1997; revised manuscript received April 2, 1998, accepted April 17, 1998.

Address for correspondence: Dr. Richard J. Bing, Huntington Medical Research Institutes, Department of Experimental Cardiology, 99 North El Molino Avenue, Pasadena, California 91101

Objectives. We sought to assess whether oxidation products of nitric oxide (NO), nitrite (NO₂^–) and nitrate (NO₃^–), referred to as NO_x, are released by the heart of patients after acute myocardial infarction (AMI) and whether NO_x can be determined in peripheral blood of these patients.

Background. Previously we reported that in experimental myocardial infarction (rabbits) NO_x is released mainly by inflammatory cells (macrophages) in the myocardium 3 days after onset of ischemia. NO_x is formed in heart muscle from NO; NO originates through the activity of the inducible form of nitric oxide synthase (iNOS).

Methods. Eight patients with acute anterior MI and an equal number of controls were studied. Coronary venous blood was obtained by coronary sinus catheterization; NO_x concentrations in coronary sinus, in arterial and peripheral venous plasma were measured. Left ventricular end-diastolic pressure was determined. Measurements were carried out 24, 48 and 72 h after onset of symptoms. The type and location of coronary arterial lesions were determined by coronary angiography. Plasma NO₃^– was reduced to NO₂^– by nitrate reductase before determination of NO₂^– concentration by chemiluminescence.

Results. The results provided evidence that in patients with acute anterior MI, the myocardial production of nitrite and nitrate (NO_x) was increased, as well as the coronary arterial–venous difference. Increased NO_x production by the infarcted heart accounted for the increase of NO_x concentration in arterial and the peripheral venous plasma. The peak elevation of NO_x occurred on days 2 and 3 after onset of the symptoms, suggesting that NO_x production was at least in part the result of production of NO by inflammatory cells (macrophages) in the heart.

Conclusions. The appearance of oxidative products of NO (NO₂^– and NO₃^–) in peripheral blood of patients with acute MI is the result of their increased release from infarcted heart during the inflammatory phase of myocardial ischemia. Further studies are needed to define the clinical value of these observations.

Abbreviations and Acronyms   AMI = acute myocardial infarction   CPK = creatine kinase   CS = coronary sinus   iNOS = inducible form of nitric oxide synthase   LAD = left anterior descending coronary artery   NO = nitric oxide   NO2– = nitrite   NO3– = nitrate   NOx = sum of nitrite and nitrate   RPP = rate pressure product

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