Earlier studies demonstrated swelling of endothelial cells in skeletal muscle capillaries during hemorrhagic shock with involvement of a pH- and amiloride-sensitive Na+/H+ antiport. The aim of this study was to determine the degree to which diminished capillary perfusion and metabolic acidosis are mechanisms for capillary narrowing. Capillary luminal diameters and micro-circulatory blood flow were measured in the rabbit tenuissimus and gastrocnemius muscles, respectively. In seven experiments, occlusion of the distal aorta produced a low-flow state in the hind limbs as assessed by laser Doppler flowmetry (LDF). The 68.5 ± 12.2% reduction in LDF flow in this local model of skeletal muscle ischemia was comparable to that in shock. After 1 h, systemic blood pH stayed the same, yet local tissue pH (venous effluent) became acidic. There was no capillary narrowing in contrast to an approximate 20% decrease in diameter found in shock. In additional experiments to simulate shock acidosis, the blood pH was reduced over 1 h by jugular vein infusion of hydrochloric acid (1.2 M, 4 ml·min-1 kg-1), with (n = 5) and without (n = 6) pre-treatment with an amiloride analog [5-(N, N-hexamethylene)amiloride] specific to block Na+/H+ exchange. Mean arterial blood pressure and LDF flow were essentially unchanged in both groups. Diameters of treated capillaries did not change, whereas those of untreated capillaries decreased by 18.0 ± 3.5% which would greatly elevate flow resistance. These results taken together suggest that systemic blood acidosis, and not low flow per se, induces a capillary narrowing which we contend is due to endothelial cell swelling.

Keywords:
Amiloride, Endothelial cell swelling, Microcirculation, No-reflow phenomenon, Skeletal muscle, Sodium-hydrogen exchange
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© 1994 S. Karger AG, Basel
1994
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