Microvascular function at the margins of early experimental myocardial infarcts in isolated rabbit hearts.

Injection of low-viscosity resin was used to identify in situ functional blood vessels at the margins of developing regional myocardial infarcts. The ventral interventricular branch (VIB) of the left coronary artery was occluded for 0-240 min in 20 isolated perfused rabbit hearts. After perfusion fixation with glutaraldehyde, resin was injected into the coronary arteries--that injected into the VIB contained dispersed lead dioxide and that injected into the remainder of the heart contained Fat Red 7B dye. This allowed macroscopic and microscopic identification of functional blood vessels. Following transmural freeze fracture, left ventricles were examined using back-scattered electron imaging in a scanning electron microscope. Close to 60% of capillaries in nonischemic myocardium allowed the passage of resin. Thirty minutes of ischemia produced a hyperemic increase to 80%-90% in the proportion of filled vessels. After 60 min, however, a severe reperfusion defect corresponding to the "no-reflow" phenomenon had developed, with virtually all vessels collapsed and less than 10% functional. Among the structurally normal myocytes adjacent to the infarct margin there was a significant reduction (to 30%-40%) in the proportion of functional capillaries. This was due to groups of dilated vessels which were not accessible to arterial supply. Although these marginal "low-flow" regions were of small volume at any one point in time, they seem likely to contribute to the progression of ischemic necrosis, and are probably nonfunctional due to the compression of their venous drainage traversing the infarct.