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)