Correlation between skeletal muscle vascular decompensation and survival: roles of tissue ischemia and innervation.

A constant-flow, cross-perfused, vascularly isolated gracilis muscle preparation was used to examine the hypothesis that locally produced and released products of ischemic muscle metabolism are responsible for the vascular decompensation (vasodilation) reported to occur in late oligemic hypotension. Well-oxygenated donor arterial blood perfused recipient gacilis muscles at a constant flow rate of 5.2 +/- 0.5 ml/100 gm/min while the recipient animals were subjected to a modified Wigger's hemorrhage protocol. Arterial and venous blood gases taken across the gracilis muscle at regular intervals during the experiments verified adequate tissue perfusion. Of the thirteen studies reported, only ten shocked recipient dogs progressed to irreversible shock postreinfusion. This series was identified as the "recipient-irreversibly shocked group." The remaining three shocked animals recovered from the shock protocol and were labeled "recipient-reversibly shocked series." The initial response to blood loss in both groups was intense vasconstriction, with the greatest initial constriction occurring in the irreversibly shocked series. The three animals that survived the protocol were able to sustain this compensatory effort, but the ten that ultimately progressed into irreversible shock postreinfusion invariably demonstrated a significant loss of vascular tone during late oligemia (conductance rose from 43% to 63% of control). Thus evidence is presented which indicates decompensation during adequate tissue perfusion, or absence of ischemia. A strong correlation was also shown to exist between sustained compensatory vasoconstriction in the gracilis muscle, and survival. The suggestion is made that part of the loss of vascular tone may be related to prejunctional inhibition of adrenergic transmission or alpha-receptor fatigue, with a minor role being played by the vasodepressor products of local tissue ischemia.