Effects of prolonged compression on the variations of haemoglobin oxygenation - assessment by spectral analysis of reflectance spectrophotometry signals.

ABSTRACT

The consequences of rhythmical flow motion for nutrition and the oxygen supply to tissue are largely unknown. In this study, the periodic variations of haemoglobin oxygenation in compressed and uncompressed skin were evaluated with a reflection spectrometer using an in vivo Sprague-Dawley rat model. Skin compression was induced over the trochanter area by a locally applied external pressure of 13.3 kPa (100 mmHg) via a specifically designed pneumatic indentor. A total of 19 rats were used in this study. The loading duration is 6 h per day for four consecutive days. Haemoglobin oxygenation variations were quantified using spectral analysis based on wavelets' transformation. The results found that in both compressed and uncompressed skin, periodic variations of the haemoglobin oxygenation were characterized by two frequencies in the range of 0.01-0.05 Hz and 0.15-0.4 Hz. These frequency ranges coincide with those of the frequency range of the endothelial-related metabolic and myogenic activities found in the flow motion respectively. Tissue compression following the above loading schedule induced a significant decrease in the spectral amplitudes of frequency interval 0.01-0.05 Hz during the pre-occlusion period on day 3 and day 4 as compared to that on day 1 (p < 0.05). In contrast, at a frequency range of 0.15-0.4 Hz, prolonged compression caused a significant increase in spectral amplitude during the pre-occlusion period in the compressed tissue on day 3 (p = 0.041) and day 4 (p = 0.024) compared to that in the uncompressed tissue on day 1. These suggested that the variations of the haemoglobin oxygenation were closely related to the endothelial-related metabolic and myogenic activities. Increased amplitude in the frequency interval 0.15-0.4 Hz indicated an increased workload of the vascular smooth muscle and could be attributed to the increase of O(2) consumption rates of arteriolar walls. The modification of vessel wall oxygen consumption might substantially affect the available oxygen supply to the compressed tissue. This mechanism might be involved in the process leading to pressure ulcer formation.