Cutaneous Mitochondrial Po2, but Not Tissue Oxygen Saturation, Is an Early Indicator of the Physiologic Limit of Hemodilution in the Pig

Abstract

Abstract Background Hemodilution is a consequence of fluid replacement during blood loss and is limited by the individual ability to compensate for decreasing hemoglobin level. We tested the ability of a novel noninvasive method for measuring cutaneous mitochondrial Po2 (mitoPo2) to detect this threshold early. Methods Anesthetized and ventilated pigs were hemodynamically monitored and randomized into a hemodilution (n = 12) or a time control (TC) group (n = 14). MitoPo2 measurements were done by oxygen-dependent delayed fluorescence of protoporphyrin IX after preparation of the skin with 20% 5-aminolevulinic acid cream. Tissue oxygen saturation (StO2) was measured with near infrared spectroscopy on the thoracic wall. After baseline measurements, progressive normovolemic hemodilution was performed in the hemodilution group in equal steps (500 ml blood replaced by 500 ml Voluven®; Fresenius Kabi AG, Germany). Consecutive measurements were performed after 20-min stabilization periods and repeated 8 times or until the animal died. Results The TC animals remained stable with regard to hemodynamics and mitoPo2. In the hemodilution group, mitoPo2 became hemoglobin-dependent after reaching a threshold of 2.6 ± 0.2 g/dl. During hemodilution, hemoglobin and mitoPo2 decreased (7.9 ± 0.2 to 2.1 ± 0.2 g/dl; 23.6 ± 2 to 9.9 ± 0.8 mmHg), but StO2 did not. Notably, mitoPo2 dropped quite abruptly (about 39%) at the individual threshold. We observed that this decrease in mitoPo2 occurred at least one hemodilution step before changes in other conventional parameters. Conclusions Cutaneous mitoPo2 decreased typically one hemodilution step before occurrence of significant alterations in systemic oxygen consumption and lactate levels. This makes mitoPo2 a potential early indicator of the physiologic limit of hemodilution and possibly a physiologic trigger for blood transfusion.