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(f)], mean effective capillary diameter [d(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(f). After 30 min of ischemia, a(f) increased 41 (Epi) and 36% (Endo). Of these percentages, fiber shortening accounted for 2 (Epi) and 25% (Endo). Decreased d(c) was correlated with increased a(f) as well as reductions in perfused capillary number and length. Whereas intracellular edema had the greatest overall effect on a(f), fiber shortening accounted for a significant increase of a(f) in Endo, where perfusion deficits were most pronounced. These data support the hypothesis that microvascular compression consequent to increased a(f) contributes to perfusion deficits after myocardial ischemia.