In Vivo and Ex Vivo Mitochondrial Function in COVID-19 Patients on the Intensive Care Unit
Lucia W. J. M. Streng,
Calvin J. de Wijs,
Nicolaas J. H. Raat,
Patricia A. C. Specht,
Dimitri Sneiders,
Mariëlle van der Kaaij,
Henrik Endeman,
Egbert G. Mik,
Floor A. Harms
Affiliations
Lucia W. J. M. Streng
Laboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands
Calvin J. de Wijs
Laboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands
Nicolaas J. H. Raat
Laboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands
Patricia A. C. Specht
Laboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands
Dimitri Sneiders
Laboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands
Mariëlle van der Kaaij
Laboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands
Henrik Endeman
Department of Intensive Care, Erasmus MC, University Medical Center Rotterdam, 3015 GD Rotterdam, The Netherlands
Egbert G. Mik
Laboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands
Floor A. Harms
Laboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands
Mitochondrial dysfunction has been linked to disease progression in COVID-19 patients. This observational pilot study aimed to assess mitochondrial function in COVID-19 patients at intensive care unit (ICU) admission (T1), seven days thereafter (T2), and in healthy controls and a general anesthesia group. Measurements consisted of in vivo mitochondrial oxygenation and oxygen consumption, in vitro assessment of mitochondrial respiration in platelet-rich plasma (PRP) and peripheral blood mononuclear cells (PBMCs), and the ex vivo quantity of circulating cell-free mitochondrial DNA (mtDNA). The median mitoVO2 of COVID-19 patients on T1 and T2 was similar and tended to be lower than the mitoVO2 in the healthy controls, whilst the mitoVO2 in the general anesthesia group was significantly lower than that of all other groups. Basal platelet (PLT) respiration did not differ substantially between the measurements. PBMC basal respiration was increased by approximately 80% in the T1 group when contrasted to T2 and the healthy controls. Cell-free mtDNA was eight times higher in the COVID-T1 samples when compared to the healthy controls samples. In the COVID-T2 samples, mtDNA was twofold lower when compared to the COVID-T1 samples. mtDNA levels were increased in COVID-19 patients but were not associated with decreased mitochondrial O2 consumption in vivo in the skin, and ex vivo in PLT or PBMC. This suggests the presence of increased metabolism and mitochondrial damage.
