THE BLOOD CELLULAR ELEMENT AS A MEDIATOR OF ISCHEMIA-REPERFUSION INJURY
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In order to explore the role of the blood cellular element in the development of reperfusion injury, the author examined whether neutrophil depletion or pretreatment with aspirin modifies infarct size and vascular resistance in the subendocardial portion of the ischemic area during reperfusion. The proximal circumflex coronary artery was occluded for 120 minutes, followed by 6 hours of reperfusion with whole blood (control group, n=7), with blood depleted of neutrophils by a neutrophil adsorption column (neutropenic group, n=7), or pretreated with aspirin (aspirin group, n=6). Severe circulatory neutropenia persisted throughout the 2-hour reperfusion period in the neutropenic group. Circumflex vascular resistance was significantly increased from the onset of reperfusion in both the control and aspirin groups. This increase in vascular resistance was prevented in the neutropenic group. Infarct size was significantly smaller in the neutropenic group than in the control group (30±5% vs. 53±8% of the risk avea, p<0.05). In the aspirin group, infarct size was 61±8 % of the risk area, a value not significantly different from that of the control group. Light and electron microscopic studies of the ischemic zone demonstrated a relative preservation of the endothelial structure of the microvasculature in the neutropenic group. In contrast, severe endothelial lesions and microvascular obstruction by neutrophils were observed in both the control and aspirin groups. These findings show that microvascular damage plays an important role in the pathogenesis of reperfusion injury and that neutrophils are important mediators of this microvascular damage.
- 北関東医学会の論文
北関東医学会 | 論文
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