SYSTEMIC BLOOD ACIDOSIS IN LOW-FLOW ISCHEMIA INDUCES CAPILLARY LUMINAL NARROWING

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 meta bolic acidosis are mechanisms for capillary narrowing. Capillary lumin al diameters and microcirculatory blood flow were measured in the rabb it tenuissimus and gastrocnemius muscles, respectively. In seven exper iments, 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 is chemia was comparable to that in shock. After 1 h, systemic blood pH s tayed the same, yet local tissue pH (venous effluent) became acidic. T here was no capillary narrowing in contrast to an approximate 20% decr ease in diameter found in shock. In additional experiments to simulate shock acidosis, the blood pH was reduced over 1 h by jugular vein inf usion of hydrochloric acid (1.2 M 4 ml.min(-1).kg(-1)), with (n = 5) a nd without (n = 6) pretreatment with an amiloride analog [5-(N,N-hexam ethylene)amiloride] specific to block Na+/H+ exchange. Mean arterial b lood pressure and LDF flow were essentially unchanged in both groups. Diameters of treated capillaries did not change, whereas those of untr eated capillaries decreased by 18.0 +/- 3.5% which would greatly eleva te flow resistance. These results taken together suggest that systemic blood acidosis, and not low flow per se, induces a capillary narrowin g which we contend is due to endothelial cell swelling.