HYPERBARIC OXYGEN IMPROVES PERIPHERAL

NERVE REGENERATION

 

Several studies have documented the effectiveness of hyperbaric oxygen in models of acute and delayed crush injury. Intermittent exposure to hyperbaric hyperoxia serves to interrupt the injury cycle of edema, ischemia and tissue necrosis(1), as well as hemorrhagic hypotension(2), which in turn leads to former edema and ischemia. Tissue ischemia is countered by the ability of hyperbaric doses of oxygen to elevate tissue oxygen tensions(3).

Furthermore, edema is reduced, secondary to hyperoxia-induced arteriolar vasoconstriction(4), leading to improved tissue viability, thereby reducing necrosis(1). Hyperbaric oxygen has also been studied in models of peripheral nerve injury(5).

Researchers from the US Air Force School Aerospace Medicine and Louisiana State University recently sought to determine what, if any, morphologic changes are associated with hyperbaric oxygen treated peripheral nerve injury(6). Their model involved a crushed sciatic nerve in the rabbit. Exposure to hyperbaric oxygen across the range of current clinical dose schedules was compared to untreated, and pressure (hyperbaric air) controls. The extent of nerve regeneration was documented via morphologic analysis of electron micrographs, by a pathologist blinded as to group.

All of the animals exposed to hyperbaric doses of oxygen were reported to demonstrate advanced stages of a healed nerve, in contrast to both control groups.

As this research was limited to a determination of regeneration of morphology, the exact effects of hyperbaric oxygen were not known. The authors speculate, however, that there may be several suggesting increased myelination, decreased edema, reduced internal collagen and improvements in neurofilamentous material density. They conclude that this study provides additional evidence of a link between tissue oxygen levels and the health of peripheral nerves.

... all animals exposed to hyperbaric oxygen "demonstrated characteristics expected of in the advanced stages of a healed nerve"

References:

  • Strauss MB et al.: Delayed use of hyperbaric oxygen for treatment of a model anterior compartment syndrome. Journal of Orthopedic Research 1986;
  • 4:108-111.
  • Skyhar MJ et al.: Hyperbaric oxygen reduces edema and necrosis of skeletal muscle in compartment syndromes associated with hemorrhagic hypotension. Journal of Bone and Joint Surgery 1986;68A:1218-1224
  • Nylander G: Tissue ischemia and hyperbaric oxygen treatment. Scand 1986; suppl. 533.
  • Nylander G et al.: Reduction of postischemic edema with hyperbaric oxygen. Plastic and Reconstructive Surgery 1985;76:595-603
  • Zamboni WA et al.: Functional evaluation of peripheral-nerve repair and the effect of hyperbaric oxygen. Journal of Reconstructive Microsurgery 1995; 11:27-29.
  • Bradshaw PO, et al.: Effect of hyperbaric oxygenation on peripheral nerve regeneration in adult male rabbits. Undersea and Hyperbaric Medicine 1996; 23(2): 107-113.
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