Cutaneous mitochondrial respirometry: non-invasive monitoring of mitochondrial function

Harms, Floor A.; Bodmer, Sander I. A.; Raat, Nicolaas J.H.; Mik, Egbert G.

doi:10.1007/s10877-014-9628-9

Cited by 24 publications

(22 citation statements)

References 32 publications

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“…Therefore, our method overcomes some of the disadvantages of earlier studies on mitochondrial dysfunction in sepsis. Because the PpIX-TSLT can be applied in humans, the technique is potentially feasible for clinical monitoring [ 32 ]. Although our implementation of the PpIX-TSLT is an important step towards addressing the need for a valid noninvasive method to monitor mitochondrial function in vivo, as proposed by Jeger et al [ 9 ], some questions still remain.…”

Section: Discussionmentioning

confidence: 99%

Non-invasive monitoring of mitochondrial oxygenation and respiration in critical illness using a novel technique

et al. 2015

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IntroductionAlthough mitochondrial dysfunction is proposed to be involved in the pathophysiology of sepsis, conflicting results are reported. Variation in methods used to assess mitochondrial function might contribute to this controversy. A non-invasive method for monitoring mitochondrial function might help overcome this limitation. Therefore, this study explores the possibility of in vivo monitoring of mitochondrial oxygen tension (mitoPO2) and local mitochondrial oxygen consumptionin in an endotoxin-induced septic animal model.MethodsAnimals (rats n = 28) were assigned to a control group (no treatment), or to receive lipopolysaccharide without fluid resuscitation (LPS-NR) or lipopolysaccharide plus fluid resuscitation (LPS-FR). Sepsis was induced by intravenous LPS injection (1.6 mg/kg during 10 min), fluid resuscitation was performed by continuous infusion of a colloid solution, 7 ml kg−1 h−1 and a 2-ml bolus of the same colloid solution. MitoPO2 and ODR were measured by means of the protoporphyrin IX-triplet state lifetime technique (PpIX-TSLT). Kinetic aspects of the drop in mitoPO2 were recorded during 60s of skin compression. ODR was derived from the slope of the mitoPO2 oxygen disappearance curve. Measurements were made before and 3 h after induction of sepsis.ResultsAt baseline (t0) all rats were hemodynamically stable. After LPS induction (t1), significant (p < 0.05) hemodynamic changes were observed in both LPS groups. At t0, mitoPO2 and ODR were 59 ± 1 mmHg, 64 ± 3 mmHg, 68 ± 4 mmHg and 5.0 ± 0.3 mmHg s−1, 5.3 ± 0.5 mmHg s−1, 5.7 ± 0.5 mmHg s−1 in the control, LPS-FR and LPS-NR groups, respectively; at t1 these values were 58 ± 5 mmHg, 50 ± 2.3 mmHg, 30 ± 3.3 mmHg and 4.5 ± 0.5 mmHg s−1, 3.3 ± 0.3 mmHg s−1, 1.8 ± 0.3 mmHg s−1, respectively. At t1, only mitoPO2 showed a significant difference between the controls and LPS-NR. In contrast, at t1 both LPS groups showed a significantly lower ODR compared to controls.ConclusionThese data show the feasibility to monitor alterations in mitochondrial oxygen consumption in vivo by PpIX-TSLT in a septic rat model. These results may contribute to the development of a clinical device to monitor mitochondrial function in the critically ill.

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Section: Discussionmentioning

confidence: 99%

Non-invasive monitoring of mitochondrial oxygenation and respiration in critical illness using a novel technique

et al. 2015

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“…Because delayed PpIX fluorescence shares the advantages of lifetime properties with phosphorescence quenching, it is equally suited for PO 2 measurements in vivo (67). The PpIX technique has been used to measure mitochondrial PO 2 (mitoPO 2 ) in the liver (67), the heart (9, 65), the skin (45,46), and the buccal mucosa (47). Importantly, deconvolution of the lifetime decay curves reveals heterogeneity of mitochondrial PO 2 levels.…”

Section: Quenching Of Delayed Ppix Fluorescencementioning

confidence: 99%

Microcirculatory and mitochondrial hypoxia in sepsis, shock, and resuscitation

İnce

Mik

2016

Journal of Applied Physiology

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After shock, persistent oxygen extraction deficit despite the apparent adequate recovery of systemic hemodynamic and oxygen-derived variables has been a source of uncertainty and controversy. Dysfunction of oxygen transport pathways during intensive care underlies the sequelae that lead to organ failure, and the limitations of techniques used to measure tissue oxygenation in vivo have contributed to the lack of progress in this area. Novel techniques have provided detailed quantitative insight into the determinants of microcirculatory and mitochondrial oxygenation. These techniques, which are based on the oxygen-dependent quenching of phosphorescence or delayed luminescence are briefly reviewed. The application of these techniques to animal models of shock and resuscitation revealed the heterogeneous nature of oxygen distributions and the alterations in oxygen distribution in the microcirculation and in mitochondria. These studies identified functional shunting in the microcirculation as an underlying cause of oxygen extraction deficit observed in states of shock and resuscitation. The translation of these concepts to the bedside has been enabled by our development and clinical introduction of hand-held microscopy. This tool facilitates the direct observation of the microcirculation and its alterations at the bedside under the conditions of shock and resuscitation. Studies identified loss of coherence between the macrocirculation and the microcirculation, in which resuscitation successfully restored systemic circulation but did not alleviate microcirculatory perfusion alterations. Various mechanisms responsible for these alterations underlie the loss of hemodynamic coherence during unsuccessful resuscitation procedures. Therapeutic resolution of persistent heterogeneous microcirculatory alterations is expected to improve outcomes in critically ill patients.

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“…Another step forward is made by the group of Harms et al, who extended their microcirculatory approach by looking “even further down the road” into the cell, more precisely into mitochondrial function [ 31 ]. The authors used a technique that was developed earlier by this group, namely the so-called Protoporphyrin IX—Triplet State Lifetime Technique.…”

Section: Monitoring the Microcirculationmentioning

confidence: 99%

Journal of Clinical Monitoring and Computing 2015 end of year summary: tissue oxygenation and microcirculation

Scheeren

2016

J Clin Monit Comput

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Last year we started this series of end of year summaries of papers published in the 2014 issues of the Journal Of Clinical Monitoring And Computing with a review on near infrared spectroscopy (Scheeren et al. in J Clin Monit Comput 29(2):217–220, 2015). This year we will broaden the scope and include papers published in the field of tissue oxygenation and microcirculation, or a combination of both entities. We present some promising new technologies that might enable a deeper insight into the (patho)physiology of certain diseases such as sepsis, but also in healthy volunteers. These may help researchers and clinicians to evaluate both tissue oxygenation and microcirculation beyond macro-hemodynamic measurements usually available at the bedside.

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Cutaneous mitochondrial respirometry: non-invasive monitoring of mitochondrial function

Cited by 24 publications

References 32 publications

Non-invasive monitoring of mitochondrial oxygenation and respiration in critical illness using a novel technique

Non-invasive monitoring of mitochondrial oxygenation and respiration in critical illness using a novel technique

Microcirculatory and mitochondrial hypoxia in sepsis, shock, and resuscitation

Journal of Clinical Monitoring and Computing 2015 end of year summary: tissue oxygenation and microcirculation

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