Abstract
In their recent paper, Protti and colleagues reported depressed oxygen consumption in patients with lactic acidosis due to biguanide intoxication and they suppose that the cause is inhibited mitochondrial respiration [1]. Another explanation for depressed oxygen consumption in these patients is also possible, however. If the blood pH is very low, glucose utilization is decreased [2] because the glycolytic enzyme phosphofructokinase is pH dependent - with decreasing pH, its activity is also decreasing [3]. Glucose utilization is an oxygen-consuming process: The consequence of decreased utilization of glucose is thus also decreased oxygen consumption. The patients reported by Protti and colleagues had on admission very low blood pH of 6.93 ± 0.20 and systemic oxygen consumption of 67 ± 28 ml/min/m2 [1]. Systemic oxygen consumption 'normalized within the next 48-72 hours' and 'Systemic O2 consumption was positively associated with arterial pH' (P < 0.001). According to Tables 2 and 3 [1], arterial pH reached normal values on days 2 to 3. Depressed oxygen consumption in patients reported by Protti and colleagues can thus be explained by their very low blood pH.
Highlights
Another explanation for depressed oxygen consumption in these patients is possible
In order to directly address the issue raised by Dr Rosival, we equipped two healthy, sedated and mechanically
The patients reported by Protti and colleagues had on admission very low blood pH of 6.93 ± 0.20 and systemic oxygen consumption of 67 ± 28 ml/min/m2 [1]
Summary
Another explanation for depressed oxygen consumption in these patients is possible, . In order to directly address the issue raised by Dr Rosival, we equipped two healthy, sedated and mechanically The consequence of decreased utilization of glucose is decreased oxygen consumption.
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