OBJECTIVE: Ischemia is a serious problem in clinical medicine, and effective methods are needed to detect ischemia before the injury becomes irreversible. In experimental studies on several organs, PCO2 was found to increase rapidly after the onset of supply-dependent anaerobic metabolism. A shortcoming of these studies was that PCO2 was not correlated with tissue concentrations of lactate and the energy status in the cell. Thus, in this study we have measured tissue concentrations of lactate, phosphocreatine, and adenosine triphosphate. We hypothesized that during ischemic conditions, PCO2 reflects lactate generation in the cell and not exhausted energy stores per se. If this is the case, PCO2 can be used to detect ischemia before the energy stores are depleted. Consequently, therapy can be instituted at a time when the organ is salvageable. DESIGN: Prospective laboratory study. SETTING: University research laboratory. SUBJECTS: Seven pigs. INTERVENTIONS: In a porcine model, gluteal skeletal muscles with no-flow ischemia were examined. PCO2 was measured both in situ and in vitro at increasing periods of time. Concomitantly, tissue lactate, adenosine triphosphate, and phosphocreatine were analyzed. MEASUREMENTS AND MAIN RESULTS: Tissue surface CO2 tension (PtCO2) increased rapidly after onset of ischemia. From a baseline of 63 +/- 3 torr (8.4 +/- 1.2 kPa) under aerobic conditions, it increased to 157 +/- 6 torr (21 +/- 2.2 kPa) after 30 mins of ischemia and 386 +/- 9 torr (51.5 +/- 3 kPa) at 120 mins. The rapid increase of PtCO2 correlated well with increasing values of lactate (r2 >.9) in the tissue. Adenosine triphosphate was essentially unchanged for 45 mins after onset of ischemia, after which it declined. Phosphocreatine decreased earlier than adenosine triphosphate in accordance with the notion that high-energy phosphate groups are transferred from phosphocreatine to adenosine triphosphate. CONCLUSION: In this porcine model of skeletal muscle ischemia, PtCO2 correlates well with tissue lactate and increases long before the energy stores of phosphocreatine and most notably adenosine triphosphate are severely reduced. Thus, PtCO2 could be monitored to detect and treat earlier stages of ischemia.
OBJECTIVE:Ischemia is a serious problem in clinical medicine, and effective methods are needed to detect ischemia before the injury becomes irreversible. In experimental studies on several organs, PCO2 was found to increase rapidly after the onset of supply-dependent anaerobic metabolism. A shortcoming of these studies was that PCO2 was not correlated with tissue concentrations of lactate and the energy status in the cell. Thus, in this study we have measured tissue concentrations of lactate, phosphocreatine, and adenosine triphosphate. We hypothesized that during ischemic conditions, PCO2 reflects lactate generation in the cell and not exhausted energy stores per se. If this is the case, PCO2 can be used to detect ischemia before the energy stores are depleted. Consequently, therapy can be instituted at a time when the organ is salvageable. DESIGN: Prospective laboratory study. SETTING: University research laboratory. SUBJECTS: Seven pigs. INTERVENTIONS: In a porcine model, gluteal skeletal muscles with no-flow ischemia were examined. PCO2 was measured both in situ and in vitro at increasing periods of time. Concomitantly, tissue lactate, adenosine triphosphate, and phosphocreatine were analyzed. MEASUREMENTS AND MAIN RESULTS: Tissue surface CO2 tension (PtCO2) increased rapidly after onset of ischemia. From a baseline of 63 +/- 3 torr (8.4 +/- 1.2 kPa) under aerobic conditions, it increased to 157 +/- 6 torr (21 +/- 2.2 kPa) after 30 mins of ischemia and 386 +/- 9 torr (51.5 +/- 3 kPa) at 120 mins. The rapid increase of PtCO2 correlated well with increasing values of lactate (r2 >.9) in the tissue. Adenosine triphosphate was essentially unchanged for 45 mins after onset of ischemia, after which it declined. Phosphocreatine decreased earlier than adenosine triphosphate in accordance with the notion that high-energy phosphate groups are transferred from phosphocreatine to adenosine triphosphate. CONCLUSION: In this porcine model of skeletal muscle ischemia, PtCO2 correlates well with tissue lactate and increases long before the energy stores of phosphocreatine and most notably adenosine triphosphate are severely reduced. Thus, PtCO2 could be monitored to detect and treat earlier stages of ischemia.