In this study, the tolerance of skeletal muscle to tourniquet application (ischemia) and to acute compartment syndrome (ischemia and pressure) was compared. In five animals, the cuff of a pneumatic tourniquet was inflated to 350 millimeters of mercury at the level of the thigh for three hours. In five other animals, an acute experimental compartment syndrome was created in one anterolateral compartment by autologous plasma infusion. The compartment pressure (measured by wick catheter) was maintained at a level equal to the mean arterial pressure for three hours. At three hours, reperfusion was established in both groups, either by tourniquet release or by decompressive fasciotomy and epimysiotomy. During both the ischemic period and a two-hour recovery period immediately thereafter, the mean intracellular pH and high-energy phosphate profile (levels of adenosine triphosphate and phosphocreatine) of the muscles of the anterolateral compartment were monitored non-invasively by phosphorus nuclear magnetic-resonance spectroscopy. Muscle biopsies were done the following day to take specimens for electron microscopic analysis of ultrastructural cellular degeneration. During ischemia, the cellular levels of phosphocreatine decreased at an identical rate in both groups. In contrast, the levels of adenosine triphosphate diminished rapidly in the animals with the compartment syndrome, but remained unchanged in the tourniquet group. Ischemic muscle acidosis was more severe in dogs with the compartment syndrome. In the tourniquet group, the phosphocreatine, adenosine triphosphate, and pH were all normal within fifteen minutes after release of the tourniquet, but these values remained depressed even two hours after fasciotomy in the group with compartment syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)