BACKGROUND: During the early stages of systemic
inflammation, the liver integrity is compromised by microcirculatory disturbances and subsequent hepatocellular injury. Little is known about the relationship between the
hemoglobin oxygen saturation (HbsO2) in sinusoids and the hepatocellular mitochondrial redox state, in early systemic
inflammation. In a murine model of early systemic
inflammation, we have explored the association between the sinusoidal HbsO2 detected with a remission spectroscopy system and 1.) the
NAD(P)H autofluorescence (an
indicator of the intracellular mitochondrial redox state) and 2.) the markers of hepatocellular injury. RESULTS: Animals submitted to 1 hour bilateral hindlimb
ischemia (I) and 3 hours of reperfusion (R) (3.0 h I/R) exhibited lower HbsO2 values when compared with
sham. Six hours I/R (1 hour bilateral hindlimb
ischemia and 6 hours of reperfusion) and the continuous infusion of
endothelin-1 (ET-1) further aggravated the
hypoxia in HbsO2. The detected
NAD(P)H autofluorescence correlated with the detected HbsO2 values and showed the same developing. Three hours I/R resulted in elevated
NAD(P)H autofluorescence compared with
sham animals. Animals after 6.0 h I/R and continuous infusion of ET-1 revealed higher
NAD(P)H autofluorescence compared with 3.0 h I/R animals. Overall the analysed HbsO2 values correlated with all markers of hepatocellular injury. CONCLUSION: During the early stages of systemic
inflammation, there is a significant decrease in hepatic sinusoidal HbsO2. In parallel, we detected an increasing
NAD(P)H autofluorescence representing an intracellular inadequate
oxygen supply. Both changes are accompanied by increasing markers of liver cell injury. Therefore, remission spectroscopy in combination with
NAD(P)H autofluorescence provides information on the
oxygen distribution, the metabolic state and the mitochondrial redox potential, within the mouse liver.