Mark Wefers Bettink

Mitochondrial oxygen monitoring during surgical repair of congenital diaphragmatic hernia or esophageal atresia: 9 175 that acts as the energy source for many cellular processes. Furthermore, mitochondria are essential for homeostasis of the cell, they play a major role in (programmed) cell death (apoptosis). Opening of the mitochondrial permeability transition pore, as a result of a stressful stimulus such as calcium or reactive oxygen species overload, leads to loss of the mitochondrial membrane potential(36). The collapse of the membrane potential results in ATP depletion and necrosis(37), and the release of mitochondrial content such as cytochrome c leads to apoptosis(38). A correlation to outcome after perturbations in cellular oxygenation have not yet been shown, but it could be used as an early warning sign. Importantly, in both a preclinical (32) and clinical setting (15) mitoPO 2 provided different information than hemoglobin saturation-based techniques like near- infrared spectroscopy (NIRS). Although visible light spectroscopy and near-infrared spectroscopy failed to show any response on a perturbation, mitoPO 2 clearly dropped. This was observed during hemodilution in piglets, where mitoPO 2 was measured simultaneously with tissue oxygen saturation on the thoracic wall. The mitoPO 2 decreased after the hemoglobin dropped below a threshold, but tissue oxygen saturation, which was measured with NIRS, did not (32). We previously published a clinical example in which mitoPO 2 showed a different response thanmicrovascular hemoglobin-saturation. Duringperipheral vasoconstriction, whichwas induced by the administration of clonidine, microvascular flow and velocity parameters measured with laser-doppler decreased both. The venous-capillary oxygen saturation did not decrease, however, mitoPO 2 in the skin measured by COMET decreased along with the decrease in flow and velocity (15). While mitoPO 2 and microvascular flow provided similar information here, we expect additional value of mitoPO 2 measurements in clinical situations in which microvascular shunting (39) and loss of hemodynamic coherence occur (40), for example in sepsis and hemodilution. During sepsis microcirculatory dysfunction occurs which causes shunting and loss of the coherence between blood flow and tissue oxygenation. Here microvascular, and ultimately mitochondrial, oxygen measurements canbe of additional value (39). The same holds true during a hyperdynamic circulation due to hemodilution, causing erythrocytes to pass too quickly through the microcirculation. This phenomenon is referred to as functional shunting and involves the inability of hemoglobin to off-load oxygen fast enough to the tissues as it passes through the microcirculation, causing cellular hypoxia while hemoglobin saturation is normal or increased (40)(41).