Abstract

The hemodynamic and metabolic consequences of microvascular occlusion, often present in the runoff bed of distal arterial reconstructions, have been difficult to quantitate clinically. To investigate these pathophysiologic relationships, a porcine hindlimb model was developed in which arteriolar patency, which we term outflow capacity, may be quantitatively defined and reduced by serial distal microembolization with 70 μm flow-directed glass bubbles. In 10 anesthetized adult pigs, hindlimb perfusion was limited to femoral artery flow (FAF) by collateral ligation. Serial measurements of outflow resistance (OR), femoral artery flow, and resting muscle pH (mpH), a metabolic index of tissue perfusion, were made as relative outflow capacity (ROC) underwent graded reduction from 1.0 (baseline) to 0 (complete occlusion). Femoral artery flow decreased linearly (FAF = 87 ROC − 3), and outflow resistance increased in hyperbolic fashion (OR = 1.66/ROC) in response to graded peripheral microembolization, whereas resting muscle pH followed a more complex relationship (ln mpH = 0.055 ROC + 1.95). An integrated analysis of these results suggests that a 50% to 60% reduction in arteriolar patency represents a critical point beyond which outflow resistance rises rapidly and hindlimb flow decreases to levels that are inadequate to support the metabolic demands of resting tissues.

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