• H M Cryer, H Kaebnick, P D Harris, and L M Flint.
• J. Surg. Res. 1985 Jul 1;39(1):59-67.

AbstractArteriolar dilatation, loss of venous tone, and uptake of shed blood characterize decompensated hemorrhagic shock. The loss of compensatory constrictor responses to hemorrhage mainly occurs in the skeletal muscle microcirculation. Tissue acidosis may be an important mediator of this phenomenon. Using a decerebrate in vivo rat cremaster muscle preparation, we observed the microcirculatory responses to hemorrhagic hypotension with cremaster bath conditions of pH 7.4 and pH 7.0. Our data indicate that tissue acidosis attenuates constrictor responses of larger arterioles (100-170 micron) and venules to hemorrhagic hypotension but has no effect on the dilator responses of small arterioles (10-30 micron). We conclude that tissue acidosis contributes significantly to loss of arteriolar resistance and to decreased venous return in the decompensatory phase of hemorrhagic shock.

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