Hyperbaric oxygen reduces edema and necrosis of skeletal muscle in compartment syndromes associated with hemorrhagic hypotension.

This study examined the effect of exposures to hyperbaric oxygen on the development of the edema and necrosis of muscle that are associated with compartment syndromes that are complicated by hemorrhagic hypotension. A compartment syndrome (twenty millimeters of mercury for six hours) was induced by infusion of autologous plasma in the anterolateral compartment of the left hind limb of seven anesthetized dogs while the mean arterial blood pressure was maintained at sixty-five millimeters of mercury after 30 per cent loss of blood volume. These dogs were treated with hyperbaric oxygen (two atmospheres of pure oxygen) and were compared with six dogs that had an identical compartment syndrome and hypotensive condition but were not exposed to hyperbaric oxygen. Forty-eight hours later, edema was quantified by measuring the weights of the muscles (the pressurized muscle compared with the contralateral muscle), and necrosis of muscle was evaluated by measuring the uptake of technetium-99m stannous pyrophosphate. The ratio for edema was significantly (p = 0.01) greater in dogs that had not been exposed to hyperbaric oxygen (1.15 +/- 0.01) than in the dogs that had been treated with hyperbaric oxygen (1.01 +/- 0.03), and the ratio for necrosis of muscle was also significantly (p = 0.04) greater in dogs that had not had hyperbaric oxygen (1.96 +/- 0.41) than in those that had been treated with hyperbaric oxygen (1.05 +/- 0.11). Comparisons were also made with the muscles of four normal control dogs and separately with the muscles of six normotensive dogs that had an identical compartment syndrome and normal blood pressure and were not treated with hyperbaric oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)

Delayed use of hyperbaric oxygen for treatment of a model anterior compartment syndrome.

This study examines the effect of delayed exposure to hyperbaric oxygen on muscle necrosis and edema development following compartment syndromes in the canine hindlimb. Compartment syndromes (100 mm Hg for 8 h) were generated in one anterolateral compartment of six anesthetized dogs. After a 2-h delay, three 1-h hyperbaric oxygen treatments (2 atm absolute pure oxygen) were given during the next 12 h. Two days later, technetium-99m stannous pyrophosphate (99mTc Sn-PYP) was injected intravenously; 3 h later, samples were obtained from the pressurized and contralateral control muscles, weighed for edema development, counted for 99mTC Sn-PYP uptake, and evaluated histologically. Hyperbaric oxygen treatments, even when delayed 2 h, reduced muscle necrosis and intramuscular edema to negligible levels (p less than 0.05) compared with untreated animals. In addition, muscle morphology remained essentially normal in all hyperbaric oxygen-treated animals. We conclude that even if hyperbaric oxygen treatments are delayed 2 h, edema and muscle necrosis are reduced significantly in a model compartment syndrome.

Value of 17beta-oestradiol in prevention of contracture formation.

Male and female rabbits were treated with 17beta-oestradiol during the 9-week development of a contracture in the left hind limb. The right hind limb served as the paired control. Untreated (absolute control) animals received saline injections. After 9 weeks biochemical analyses of water, hexosamine, soluble and total collagen, as well as biomechanical measurements of joint stiffness, were performed on the dissected knees. In all cases 17beta-oestradiol reduced the measured stiffness in the contractures by approximately 50% as compared to the contractures of the untreated animals. 17beta-oestradiol, in addition, partially prevented the loss of water and hexosamine which occurs in untreated contractures. 17beta-oestradiol administration also decreased the content of soluble collagen fractions in the periarticular connective tissue of both the control and experimental knees. The relationship of these biochemical findings to their mechanical consequences is discussed, and the results are related to a working hypothesis of stress- and motion-dependent homoeostasis within periarticular connective tissue.