scholarly journals Mitochondrial oxygen monitoring with COMET: verification of calibration in man and comparison with vascular occlusion tests in healthy volunteers

Author(s):  
R. Ubbink ◽  
M. A. Wefers Bettink ◽  
W. van Weteringen ◽  
E. G. Mik

Abstract Mitochondria are the primary consumers of oxygen and therefore an important location for oxygen availability and consumption measurement. A technique has been developed for mitochondrial oxygen tension (mitoPO2) measurement, incorporated in the COMET. In contrast to most textbooks, relatively high average mitoPO2 values have been reported. The first aim of this study was to verify the validity of the COMET calibration for mitoPO2 measurements in human skin. The second aim was to compare the dynamics of mitoPO2 to several other techniques assessing tissue oxygenation. Firstly, we performed a two-point calibration. Mitochondrial oxygen depletion was achieved with vascular occlusion. A high mitoPO2 was reached by local application of cyanide. MitoPO2 was compared to the arterial oxygen partial pressure (PaO2). Secondly, for deoxygenation kinetics we compared COMET variables with the LEA O2C, SenTec OxiVenT™ and Medtronic INVOS™ parameters during a vascular occlusion test. 20 healthy volunteers were recruited and resulted in 18 datasets (2 times 9 subjects). The lowest measured mitoPO2 value per subject had a median [IQR] of 3.0 [1.0–4.0] mmHg, n = 9. After cyanide application the mitoPO2 was 94.1 mmHg [87.2–110.9] and did not differ significantly (n = 9, p = 0.5) from the PaO2 of 101.0 [98.0–106.0] mmHg. In contrast to O2C, OxiVenT™ and INVOS parameters, mitoPO2 declined within seconds with pressure on the probe. The kinetics from this decline are used to mitochondrial oxygen consumption (mitoVO2). This study validates the calibration of the COMET device in humans. For mitoVO2 measurements not only blood flow cessation but application of local pressure is of great importance to clear the measurement site of oxygen-carrying erythrocytes.

2016 ◽  
Vol 39 (3) ◽  
pp. 1068-1077 ◽  
Author(s):  
Rosi Bissinger ◽  
Daniela S. Kempe-Teufel ◽  
Sabina Honisch ◽  
Syed M. Qadri ◽  
Elko Randrianarisoa ◽  
...  

Background/Aims: Arteritis is an inflammatory disease of the vascular wall leading to ischemia and vascular occlusion. Complications of arteritis include anemia, which could, at least in theory, result from suicidal erythrocyte death or eryptosis, which is characterized by erythrocyte shrinkage and phosphatidylserine (PS) exposure at the erythrocyte surface. Cellular mechanisms involved in the stimulation of eryptosis include increased cytosolic Ca2+-concentration ([Ca2+]i), oxidative stress and ceramide formation. The present study explored whether and how arteritis influences eryptosis. Methods: Blood was drawn from patients suffering from arteritis (n=17) and from healthy volunteers (n=21). PS exposure was estimated from annexin V-binding, erythrocyte volume from forward scatter, [Ca2+]i from Fluo3-fluorescence, reactive oxygen species (ROS) from DCFDA fluorescence and ceramide abundance from FITC-conjugated antibody binding in flow cytometry. The patients suffered from anemia despite 2.8±0.4% reticulocytes. Results: The percentage of PS-exposing erythrocytes was significantly higher in patients (1.1±0.1%) than in healthy volunteers (0.3±0.1%). The increase in PS exposure was paralleled by increase in oxidative stress and [Ca2+]i but not by significant changes of ceramide abundance. Erythrocyte PS exposure and ROS production were significantly enhanced in erythrocytes exposed to patient plasma as compared to exposure to plasma from healthy volunteers. Conclusion: Arteritis is associated with enhanced eryptosis due to increased [Ca2+]i and oxidative stress. The eryptosis contributes to or even accounts for the anemia in those patients. As eryptotic erythrocytes adhere to endothelial cells of the vascular wall, they could impede microcirculation and thus contribute to vascular occlusion.


2020 ◽  
Vol 57 (6) ◽  
pp. 341-347
Author(s):  
Jaeyeon Chung ◽  
Sang-Hwan Ji ◽  
Young-Eun Jang ◽  
Eun-Hee Kim ◽  
Ji-Hyun Lee ◽  
...  

Near-infrared spectroscopy devices can measure peripheral tissue oxygen saturation (StO<sub>2</sub>). This study aims to compare StO<sub>2</sub> using INVOS® and different O3™ settings (O3<sup>25:75</sup> and O3<sup>30:70</sup>). Twenty adults were recruited. INVOS® and O3™ probes were placed simultaneously on 1 side of forearm. After baseline measurement, the vascular occlusion test was initiated. The baseline value, rate of deoxygenation and reoxygenation, minimum and peak StO<sub>2</sub>, and time from cuff release to peak value were measured. The parameters were compared using ANOVA and Kruskal-Wallis tests. Bonferroni’s correction and Mann-Whitney pairwise comparison were used for post hoc analysis. The agreement between StO<sub>2</sub> of devices was evaluated using Bland-Altman plots. INVOS® baseline value was higher (79.7 ± 6.4%) than that of O3<sup>25:75</sup> and O3<sup>30:70</sup> (62.4 ± 6.0% and 63.7 ± 5.5%, respectively, <i>p</i> &#x3c; 0.001). The deoxygenation rate was higher with INVOS® (10.6 ± 2.1%/min) than with O3<sup>25:75</sup> and O3<sup>30:70</sup> (8.4 ± 2.2%/min, <i>p</i> = 0.006 and 7.5 ± 2.1%/min, <i>p</i> &#x3c; 0.001). The minimum and peak StO<sub>2</sub> were higher with INVOS®. No significant difference in the reoxygenation rate was found between the devices and settings. The time to reach peak after cuff deflation was faster with INVOS® (both <i>p</i> &#x3c; 0.001). Other parameters were similar. There were no differences between the different O3™ settings. There were differences in StO<sub>2</sub> measurements between the devices, and these devices should not be interchanged. Differences were not observed between O3™ device settings.


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