Role of leukocytes in coronary vascular endothelial injury due to ischemia and reperfusion.
- 1 December 1991
- journal article
- abstracts
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 69 (6) , 1566-1574
- https://doi.org/10.1161/01.res.69.6.1566
Abstract
A possible cause of the coronary endothelial injury that occurs with ischemia and reperfusion is the local accumulation of leukocytes during these events. To investigate the role of leukocytes in coronary endothelial injury, we tested the effect of leukocyte removal by filtering on coronary endothelial function in a canine model of regional myocardial ischemia and reperfusion. Blood was supplied to the left anterior descending and circumflex arteries of anesthetized dogs via an extracorporeal circulation. A 60-minute left anterior descending occlusion was followed by 120 minutes of reperfusion either with (n = 6) or without (n = 6) leukocyte filters in the extracorporeal circuit. Regional myocardial blood flow was measured with radiolabeled microspheres. Radiolabeled autologous transferrin (113mIn) and erythrocytes (99mTc) were given intravenously during reperfusion for assessment of microvascular permeability. Left anterior descending and circumflex coronary artery rings were assessed in vitro for endothelium-dependent dilation to acetylcholine, ADP, and thrombin. In unfiltered dogs, ischemia and reperfusion increased the protein leak index of ischemic myocardium 2.3-fold compared with that of nonischemic myocardium (2.3 +/- 0.5 to 5.2 +/- 1.6, p less than 0.05). In filtered dogs, there was no difference in the protein leak index of nonischemic versus ischemic myocardium (1.5 +/- 0.4 versus 1.9 +/- 0.5, p = NS). There was impaired left anterior descending coronary artery relaxation (versus circumflex) in response to endothelium-dependent vasodilators in vitro. However, relaxation was not consistently improved by leukocyte filtering. We conclude that leukocytes are responsible for the endothelial injury secondary to ischemia and reperfusion in the coronary microvasculature but have little or no effect on the endothelial injury in epicardial coronary arteries.Keywords
This publication has 15 references indexed in Scilit:
- Do leukocytes have a role in the cerebral no-reflow phenomenon?Journal of Neurology, Neurosurgery & Psychiatry, 1989
- Reduction in coronary vasodilator reserve following coronary occlusion and reperfusion in anesthetized dog: Role of endothelium-derived relaxing factor, myocardial neutrophil infiltration and prostaglandinsJournal of Molecular and Cellular Cardiology, 1988
- Neutrophils as potential participants in acute myocardial ischemia: Relevance to reperfusionJournal of the American College of Cardiology, 1988
- Reduction of experimental canine myocardial reperfusion injury by a monoclonal antibody (anti-Mo1, anti-CD11b) that inhibits leukocyte adhesion.Journal of Clinical Investigation, 1988
- Reperfusion after acute coronary occlusion in dogs impairs endothelium-dependent relaxation to acetylcholine and augments contractile reactivity in vitro.Journal of Clinical Investigation, 1987
- Oxygen-Derived Free Radicals in Postischemic Tissue InjuryNew England Journal of Medicine, 1985
- Coronary Vascular Reactivity After Acute Myocardial IschemiaScience, 1982
- Measurement of Cutaneous Inflammation: Estimation of Neutrophil Content with an Enzyme MarkerJournal of Investigative Dermatology, 1982
- Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.Journal of Clinical Investigation, 1978
- The “No-Reflow” Phenomenon after Temporary Coronary Occlusion in the DogJournal of Clinical Investigation, 1974