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  Vol. 129 No. 10, October 1994 TABLE OF CONTENTS
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Effect of Hyperbaric Oxygen and Growth Factors on Rabbit Ear Ischemic Ulcers

Lily L. Zhao, MD; John D. Davidson, MD; Sang Chin Wee, MD; Sanford I. Roth, MD; Thomas A. Mustoe, MD

Arch Surg. 1994;129(10):1043-1049.


Abstract



Objective
To test the influence of hyperbaric oxygen (HBO), platelet-derived growth factor—BB (PDGF-BB), and transforming growth factor–β1 (TGF-β1) on the deficit in wound healing produced by ischemia in a noncontractive dermal ulcer standardized model in the rabbit ear.

Design and Interventions
Dermal ulcers were created in the ischemic ears of 42 anesthetized young female New Zealand white rabbits. The controls were ulcers created in nonischemic ears of eight anesthetized young female New Zealand white rabbits. Either PDGF-BB (5 µg), TGF-β1 (1 µg), or buffer alone was applied to each wound, which was then covered. Some groups were treated with HBO on days 0 through 4. Wounds were harvested on day 7 and were evaluated histologically.

Main Outcome Measures
The amount of epithelial regrowth and granulation tissue production were measured. The wounds were evaluated for glycosaminoglycan and collagen content. Angiogenesis was measured.

Results
Hyperbaric oxygen alone, in the ischemic model, increased the production of new granulation tissue by approximately 100% at 7 days without significantly affecting new epithelial growth (P=.03). In contrast, PDGF-BB and TGF-β1 each increased the new granulation tissue volume by greater than 200% in 7 days (P=.0001) and also had a statistically significant effect on new epithelial growth. However, the addition of growth factors to HBO treatment produced a synergistic total reversal of the wound-healing deficit produced by ischemia (P=.0001).

Conclusions
Both PDGF-BB and TGF-β1 alone are more effective than HBO treatment by itself in accelerating the impaired wound healing produced by ischemia. However, the combination of HBO with either of the growth factors has a synergistic effect that totally reverses the deficit produced by ischemia.

(Arch Surg. 1994;129:1043-1049)



Author Affiliations



From the Division of Plastic Surgery (Drs Zhao and Mustoe) and the Department of Pathology (Dr Roth), Northwestern University School of Medicine, Chicago, Ill, the Division of Hyperbaric Medicine, St Luke's Hospital, and the Department of Medicine, Washington University School of Medicine, St Louis, Mo (Dr Davidson), and the Department of Plastic Surgery, Catholic University Medical School, Seoul, Korea (Dr Wee).



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