Evidence is mounting that susceptibility to pressure ulcers in the spinal cord injured is due to the interactive effects of prolonged immobilization and injury-related autonomic dysfunction associated with reduced tissue perfusion. To determine whether tissue oxygenation at the sacrum is reduced in spinal cord injury, we compared transcutaneous oxygen tension (PtcO2) levels in 21 subjects with spinal cord injury and 11 able-bodied controls lying prone and supine on egg-crate mattresses. Spinal cord injured subjects above and below the median supine PtcO2 value were also compared in terms of the presence or absence of pressure ulcers. The PtcO2 level of the spinal cord injured (mean +/- SD) was lower than that of the controls in the prone position (65.3 +/- 16mmHg vs 76.4 +/- 13mmHg; F = 3.9, df = 1, p = .053), and markedly lower in the supine position (49.1 +/- 26mmHg versus 74.2 +/- 10mmHg; F = 9.7, df = 1, p = .004). Examination of mean PtcO2 levels over time showed that those of the controls fell slightly following supination but returned to the previous level within 15 minutes. In contrast, those of the spinal cord injured fell rapidly by 18mmHg and stabilized after 15 minutes at a level 27mmHg below that of the controls. Five of the 10 (50%) spinal cord injured subjects with PtcO2 levels below the median supine PtcO2 level had a pressure ulcer compared to one among the 11 (9%) spinal cord injured subjects with PtcO2 levels above the median (p = .055, by Fisher's exact test). These results suggest the need for further studies on the role of reduced tissue oxygenation in the etiology of pressure ulcers.