LAUSR

ABSTRACT Evidence suggests that propofol infusion syndrome (PRIS) is caused by an altered mitochondrial function. The aim of this study was to examine the effects of propofol and the vehicle MCT on mitochondrial function in hepatic and colonic tissue. Mitochondrial oxygen consumption was determined in colon and liver homogenates after incubation with buffer (control), propofol (50, 75, 100, 500 &mgr;M) or the carrier substances DMSO and MCT. State 2 (substrate‐dependent) and state 3 (ADP‐dependent respiration) were assessed. RCI (respiratory control index) ‐ an indicator for coupling between electron transport chain system (ETS) and oxidative phosphorylation (OXPHOS) and ADP/O ratio ‐ a parameter for efficacy of OXPHOS were calculated. Data were presented as % of control. In hepatic mitochondria, 500 &mgr;M propofol reduced RCI formulation‐independently (propofol/MCT 500 &mgr;M: complex I: 66.3 ± 8.7%*, complex II: 75.5 ± 9.2%*; propofol/DMSO 500 &mgr;M: complex I: 29.1 ± 8.8%*, complex II: 49.3 ± 15.5%*). 75 &mgr;M Propofol/MCT reduced ADP/O for complex I (73.5 ± 27.3%*). DMSO did not affect hepatic mitochondria whereas MCT reduced RCI for complex II (87.2 ± 9.8%*) and ADP/O for complex I (93.7 ± 31.7%*). In colon 50 &mgr;M Propofol/MCT increased RCI for complex I and II (complex I: 127.2 ± 10.7%*, complex II: 136.8 ± 33.9%*) and 100 &mgr;M Propofol/MCT for complex I (131.4 ± 18.7%*). 500 &mgr;M Propofol/DMSO increased ADP/O for complex I (139.4 ± 41.4%*). DMSO did not affect RCI but increased ADP/O for both complexes (complex I: 119.9 ± 25.8%*, complex II: 110.2 ± 14.2%*). MCT increased RCI for complex I (123.0 ± 31.6%*). In hepatic mitochondria propofol uncoupled ETS from OXPHOS formulation‐independently and propofol/MCT reduced efficacy of OXPHOS. In colonic mitochondria, propofol/MCT strengthened the coupling and propofol/DMSO enhanced the efficacy of OXPHOS.