Extracellular-intracellular lactate gradients in skeletal muscle during hemorrhagic shock in the rat.

Previous studies performed in our laboratory with a constant-pressure model of hemorrhagic shock in the anesthetized rat have failed to find any significant effect of shock on the glycogen or high-energy phosphate content of the soleus muscle that would be consistent with inadequate oxygen supply. The present study examined the extracellular-intracellular lactate concentration gradients under conditions identical to those of our previous studies to determine whether skeletal muscle lactate accumulation might occur under these conditions. Twenty-seven pentobarbital-anesthetized rats were bled to a mean arterial blood pressure of 40 mm Hg during a 10-minute period and maintained at that level by withdrawal or reinfusion of shed blood. Arterial blood samples were taken and soleus muscles rapidly frozen during four defined phases of hemorrhagic shock: the early compensatory (phase I), maximal compensatory (phase II), early decompensatory (phase III), and late decompensatory (phase IV) phases. The results showed that although the plasma lactate and intracellular lactate concentrations change in parallel during all phases of shock, the extracellular--intracellular concentration gradient for lactate was always positive, ranging from 0.64 +/- 0.61 mmol/L in phase I to 6.41 +/- 0.93 mmol/L in phase III. These findings, together with the previous failure to find significant high-energy phosphate or glycogen changes in the soleus muscle, suggest that this skeletal muscle is not metabolizing anaerobically and does not contribute to the observed lactic acidemia in this model of hemorrhagic shock.