MICROVASCULAR COMPRESSION DURING MYOCARDIAL-ISCHEMIA - MECHANISTIC BASIS FOR NO-REFLOW PHENOMENON

Alterations in fiber size and capillary diameter were highly correlated with perfusion deficits after myocardial ischemia. After 5 (n = 3) and 30 (n = 5) min of global normothermic ischemia, isolated rabbit hearts were perfused with India ink and then with glutaraldehyde. Morphometric techniques were used to determine mean fiber cross-sectional area [(a) over bar(f)], mean effective capillary diameter [(d) over bar(c)], total and perfused capillary number per fiber area, and capillary length per fiber volume in subepicardium (Epi) and subendocardium (Endo). Sarcomere length was measured to differentiate between effects of fiber shortening and intracellular edema on (a) over bar(f). After 30 min of ischemia, (a) over bar(f) increased 41 (Epi) and 36% (Endo). Of these percentages, fiber shortening accounted for 2 (Epi) and 25% (Endo). Decreased (d) over bar(c) was correlated with increased (a) over bar(f) as well as reductions in perfused capillary number and length. Whereas intracellular edema had the greatest overall effect on (a) over bar(f), fiber shortening accounted for a significant increase of (a) over bar(f) in Endo, where perfusion deficits were most pronounced. These data support the hypothesis that microvascular compression consequent to increased (a) over bar(f) contributes to perfusion deficits after myocardial ischemia.