Stability of 8-, 15-, and 26-micron microspheres entrapped in feline myocardium
- 1 January 1983
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 244 (1) , H121-H130
- https://doi.org/10.1152/ajpheart.1983.244.1.h121
Abstract
The stability of 8-, 15-, and 26-micron radioactive microspheres entrapped in ischemic and nonischemic myocardium and possible mechanisms for microsphere loss were investigated. Anesthetized cats were given microspheres prior to left anterior descending coronary artery occlusion (or sham operation) and 8 h later. Eight-micron microspheres, compared with 15-micron spheres, underestimated preocclusion myocardial blood flow in ischemic and nonischemic tissue by 30%. With 26-micron spheres, endocardial-to-epicardial blood flow ratio was 1.28. In nonischemic tissue, no loss of 15- and 26-micron microspheres occurred during 8 h. In ischemic myocardium, however, 15% apparent loss of 15- and 26-micron preocclusion spheres took place. In endocardial ischemic tissue, edema could account for 50% of the 15-micron microsphere loss and almost completely for loss of 26-micron spheres. In epicardial ischemic tissue, microsphere loss was not influenced by edema. We found no hemodynamic variable that could predict the magnitude of microsphere loss. Only weak evidence for migration of 15- and 26-micron microspheres through lymphatic pathways was found. Most likely the spheres migrated through venous pathways to embolize in the lungs. We conclude that 15-micron microspheres provide the most reliable tissue blood flow estimates in normal myocardium, but even for these spheres significant loss occurs during 8 h of ischemia.This publication has 2 references indexed in Scilit:
- Effects of infarcted myocardium on regional blood flow measurements to ischemic regions in canine heart.Circulation Research, 1980
- The changing anatomic reference base of evolving myocardial infarction. Underestimation of myocardial collateral blood flow and overestimation of experimental anatomic infarct size due to tissue edema, hemorrhage and acute inflammation.Circulation, 1979