Neutrophil depletion fails to modify myocardial no reflow and functional recovery after coronary reperfusion

• Published in: Journal of the American College of Cardiology Vol. 14; no. 7; pp. 1803 - 1813
• Main Authors: Carlson, Robert E., Schott, Robert J., Buda, Andrew J.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.12.1989; Elsevier Science
• Subjects: Animals; Biological and medical sciences; Cardiology. Vascular system; Coronary Circulation; Coronary heart disease; Dogs; Echocardiography; Heart; Hemodynamics; Medical sciences; Myocardial Infarction - pathology; Myocardial Reperfusion; Neutrophils - physiology; Fissipedia; Animal model; Carnivora; Cardiovascular disease; Blood flow; Vertebrata; Mammalia; Reperfusion; Ischemia; Animal; Myocardium; Hemodynamics; Dog; Neutropenia
• DOI: 10.1016/0735-1097(89)90036-3
• ISSN: 0735-1097

Recent studies suggest that neutrophil accumulation and activation in postischemic myocardium may be responsible for myocardial no reflow, which is characterized by an incomplete restoration of blood flow after reperfusion. To examine this further, 11 open chest, anesthetized dogs received bolus injections of a bovine neutrophil antiserum that produced an average 81 ± 5% depletion of circulating neutrophils, and 10 control dogs received nonimmune serum. Each animal underwent 2 h of left circumflex artery occlusion followed by 4 h of reperfusion. Simultaneous two-dimensional echocardiography and radioactive microsphere blood flow studies were performed at baseline, 2 h of occlusion and early (∼5 min) and 4 h of reperfusion. During occlusion, both groups developed similar reductions in myocardial blood flow and levels of ischemic zone myocardial wall thinning. At early reperfusion, similar levels of hyperemia and regional hypokinesia were observed for both groups. By late reperfusion, both groups experienced significant no reflow in the subendocardium (p < 0.05) and reduced reflow in the mid-myocardium. Regional depression in ischemic zone function persisted throughout the reperfusion period in both groups. However, infarct size expressed as a percent of left ventricular weight, assessed by triphenyltetrazolium chloride staining, was smaller for the neutrophil depletion group compared with the control group (8.7 ± 1.3% versus 13.1 ± 1.8%, p < 0.05). It is concluded that an 81% neutrophil depletion fails to modify the no reflow phenomenon or improve functional recovery after 2 h of coronary artery occlusion and 4 h of coronary reperfusion despite modification of the ultimate size of necrosis.