In a study on rats, long-tern intermittent
hyperbaric oxygenation at 2 ATA had no effect on the healing rate of open
wounds in which the circulation was left intact. When the
wound edges were devascularized, however, hyperbaric
oxygen enhanced the
wound closure rate in the final stages of healing, thus counteracting the delay caused by disturbed blood supply. During the hyperbaric exposure, tissue
pO-2 increased considerably in both normal and devascularized skin, whereas tissue pCO-2 increased only slightly. Combined systemic and local
hypoxia--12%
oxygen at 1 atm--retarded the closure rate of full-thickness skin
wounds. This was noted both in acclimatized and in unacclimatized rats. Thirteen-day adaptation to
hypoxia increased the healing rate and subcutaneous tissue
pO-2 to normal levels, but when
hypoxia was continued, tissue
pO-2 and the
wound closure rate decreased markedly. This was probably due to a decreased blood flow induced by secondary
erythrocytosis and an elevated blood viscosity.