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 microcirculatory 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) pretreatment 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.