Reduction of skeletal muscle necrosis using intermittent hyperbaric oxygen in a model compartment syndrome.

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Abstract
To study the effect of intermittent exposures to hyperbaric O2 on experimentally induced compartment syndrome in the hind limbs of 12 dogs, a compartment syndrome was produced by infusion of autologous plasma during general anesthesia. Intracompartmental pressures, monitored with wick and slit catheters, were maintained at 30, 60 or 100 mm of Hg for 8 h in 3 groups of dogs. Immediately after the infusion was stopped, each dog was placed in a monoplace hyperbaric chamber that was pressurized to 2 atmospheres absolute for 1 h. During the next 10 h the same dogs received 2 additional 1-h exposures to hyperbaric O2, with a 4-h break between each exposure. After the infusion (48 h), skeletal muscle necrosis was quantified by i.v. injection of 99mTc stannous pyrophosphate. Three h later, each dog was killed and samples from the pressurized and control anterior-compartment muscles were processed for histological examination and counted for uptake of the Tc. The results were compared with the findings in 25 dogs that were not exposed to hyperbaric O2 after infusion. Muscle necrosis, quantified by uptake of Tc-99m, was significantly reduced (P < 0.01) after exposures to hyperbaric O2 as compared with the necrosis that was produced in muscles of dogs that were not exposed to hyperbaric O2. Treatments with hyperbaric O2 effectively reduced edema in the experimental compartment. At 100 mm of Hg the ratio of the weight of the muscles from the experimental anterolateral compartment to the weight of the muscles from the control anterolateral compartment of the opposite limb was significantly less (P < 0.05) than the same ratio in the dogs that did not receive hyperbaric O2. Histological evaluations of muscle damage closely correlated with the pyrophosphate uptakes. Hyperbaric O2 significantly reduces muscle damage in experimentally produced compartment syndrome in dogs.