Effect of a critical coronary stenosis on myocardial neutrophil accumulation during ischemia and early reperfusion in dogs

Journal Article · Fri Dec 01 00:00:00 EST 1989 · Circulation; (USA)

DOI:https://doi.org/10.1161/01.CIR.80.6.1805· OSTI ID:6983826

Richard, V J; Brooks, S E; Jennings, R B; Reimer, K A ^[1]

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1. Duke Univ. Medical Center, Durham, NC (USA)

In many experimental models of ischemia and reperfusion, reperfusion is performed abruptly, allowing full reactive hyperemia to occur. In the clinical setting, however, reperfusion after thrombolysis is often limited by residual stenosis. Some experimental models attempt to mimic this situation with a critical stenosis. The purpose of this study was to determine whether preventing reactive hyperemia during the initial phase of reperfusion would modify the transmural distribution of myocardial blood flow or the myocardial accumulation of polymorphonuclear leukocytes (PMNs). The left circumflex artery was occluded for 90 minutes and then reperfused for 60 minutes in anesthetized, open-chest dogs. Autologous PMNs were isolated, labeled with 111In, and reinjected 1 hour before coronary occlusion. 125I-labeled albumin was injected simultaneously to correct for 111In associated with plasma proteins and to permit calculation of the number of PMNs in the inner, middle, and outer thirds of nonischemic and ischemic-reperfused tissue. The presence of a critical stenosis abolished reactive hyperemia during the first 5 minutes of reperfusion, but did not substantially affect blood flow measured after 55 minutes of reperfusion. In both groups, there was a significant accumulation of PMNs in all layers of the ischemic-reperfused bed compared with the nonischemic bed, and the magnitude of this PMN accumulation was not altered by the presence of a critical stenosis. Moreover, infarct size, estimated by triphenyl tetrazolium chloride (TTC) loss after 60 minutes of reperfusion, was not affected by the presence of a critical stenosis. Thus, the presence of a critical stenosis abolished the hyperemic blood flow after reperfusion but did not influence the early PMN response to ischemia and reperfusion or the early loss of TTC staining.

• OSTI ID: 6983826
• Journal Information: Circulation; (USA), Vol. 80:6; ISSN 0009-7322
• Country of Publication: United States
• Language: English

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62 RADIOLOGY AND NUCLEAR MEDICINE
MYOCARDIUM
BLOOD FLOW
NEUTROPHILS
BIOLOGICAL ACCUMULATION
ALBUMINS
CORONARIES
DOGS
INDIUM 111
IODINE 125
ISCHEMIA
PERFUSED TISSUES
ANIMAL TISSUES
ANIMALS
ARTERIES
BETA DECAY RADIOISOTOPES
BIOLOGICAL MATERIALS
BLOOD
BLOOD CELLS
BLOOD VESSELS
BODY
BODY FLUIDS
CARDIOVASCULAR DISEASES
CARDIOVASCULAR SYSTEM
DAYS LIVING RADIOISOTOPES
DISEASES
ELECTRON CAPTURE RADIOISOTOPES
HEART
INDIUM ISOTOPES
INTERMEDIATE MASS NUCLEI
IODINE ISOTOPES
ISOMERIC TRANSITION ISOTOPES
ISOTOPES
LEUKOCYTES
MAMMALS
MATERIALS
MINUTES LIVING RADIOISOTOPES
MUSCLES
NUCLEI
ODD-EVEN NUCLEI
ORGANIC COMPOUNDS
ORGANS
PROTEINS
RADIOISOTOPES
TISSUES
VASCULAR DISEASES
VERTEBRATES
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