Conclusion
These 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.
Methods
Animals (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.
Results
At 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.