Previous reports indicate that hyperoxemia disturbs the striated muscle tissue oxygenation in both critically ill patients and in healthy human volunteers. We believe that further studies of this problem can most conveniently be carried out in an animal model. A systematic study on the influence of higher than normal arterial pO2 levels on striated muscle surface tissue oxygen pressure distributions (OPD) was performed using an MDO oxygen electrode. Experiments were carried out during controlled ventilation in a rabbit model conceived to maintain exceptional cardiovascular stability. The PaO2 level was varied by altering FiO2 (the fraction of inspired oxygen) randomly between 0.21 (mean PaO2 10.7 kPa), 0.30 (mean PaO2 19.2 kPa), 0.5 (mean PaO2 29.1 kPa) and 0.70 (mean PaO2 44.0 kPa) with only small variations in PaCO2 (4-5 kPa). There was a clear relationship between the degree of hyperoxemia and the degree of abnormality of the muscle tissue OPD: the higher the PaO2 level, the more abnormal was the muscle tissue OPD. Slightly disturbed (scattered) muscle tissue OPD:s appeared at PaO2 levels around 19 kPa, while increasingly scattered OPD:s appeared at PaO2 29 kPa and 44 kPa, respectively. At normal baseline PaO2 levels (mean PaO2 10.7 kPa) muscle OPD:s were normal. The time needed to achieve stable muscle tissue oxygen pressure levels after PaO2 had been increased was longer than expected, i.e., on average 45 min. The OPD shapes as well as the mode of reaction to hyperoxemia were found to be the same in the rabbit as in man. Our model displayed good macro- and microvascular stability and should be useful for studies on regulatory mechanisms of skeletal muscle oxygenation.
|Original language||English (US)|
|Number of pages||24|
|Journal||Microcirculation, endothelium, and lymphatics|
|State||Published - Apr 1988|
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