OBJECTIVE: Mitochondrial cytochrome a,a3 redox shifts can be determined by near-infrared wavelength reflection. Since near-infrared wavelengths penetrate skin and bone, a potential exists to noninvasively measure mitochondrial oxidation using this phenomenon. The purpose of this study was to compare conventional parameters of resuscitation with regional measurements of spectroscopically derived cytochrome redox state in a hemorrhagic shock model. DESIGN: Prospective, controlled laboratory investigation. SETTING: Animal research laboratory of a university medical center. SUBJECTS: New Zealand white rabbits (n = 23), weighing 2 to 3 kg. INTERVENTIONS: After anesthesia and instrumentation, the subjects underwent laparotomy with placement of near-infrared spectroscopy probes on the stomach, liver, kidney, and hamstring muscle. Baseline measurements were obtained, and phlebotomy was used to reduce cardiac output by 60% for 30 mins. Animals were resuscitated with shed autologous blood and crystalloid to reach baseline cardiac output (0.9%), and were monitored for an additional 60 mins. MEASUREMENTS AND MAIN RESULTS: Significant correlations between mitochondrial cytochrome a,a3 redox state, cardiac output, and oxygen delivery were observed throughout shock and resuscitation. However, gastric cytochrome oxidation did not recover after shock, despite systemic evidence of adequate resuscitation (p < .05). CONCLUSIONS: Resuscitation from severe hemorrhagic shock may not uniformly restore cellular oxygenation, despite normalization of traditional parameters of resuscitation. Direct monitoring of cytochrome oxidation may be useful in identifying regional areas of dysoxia.
OBJECTIVE: Mitochondrial cytochrome a,a3 redox shifts can be determined by near-infrared wavelength reflection. Since near-infrared wavelengths penetrate skin and bone, a potential exists to noninvasively measure mitochondrial oxidation using this phenomenon. The purpose of this study was to compare conventional parameters of resuscitation with regional measurements of spectroscopically derived cytochrome redox state in a hemorrhagic shock model. DESIGN: Prospective, controlled laboratory investigation. SETTING: Animal research laboratory of a university medical center. SUBJECTS: New Zealand white rabbits (n = 23), weighing 2 to 3 kg. INTERVENTIONS: After anesthesia and instrumentation, the subjects underwent laparotomy with placement of near-infrared spectroscopy probes on the stomach, liver, kidney, and hamstring muscle. Baseline measurements were obtained, and phlebotomy was used to reduce cardiac output by 60% for 30 mins. Animals were resuscitated with shed autologous blood and crystalloid to reach baseline cardiac output (0.9%), and were monitored for an additional 60 mins. MEASUREMENTS AND MAIN RESULTS: Significant correlations between mitochondrial cytochrome a,a3 redox state, cardiac output, and oxygen delivery were observed throughout shock and resuscitation. However, gastric cytochrome oxidation did not recover after shock, despite systemic evidence of adequate resuscitation (p < .05). CONCLUSIONS: Resuscitation from severe hemorrhagic shock may not uniformly restore cellular oxygenation, despite normalization of traditional parameters of resuscitation. Direct monitoring of cytochrome oxidation may be useful in identifying regional areas of dysoxia.
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