Dual Component Analysis for In Vivo T₂* Decay of Hyperpolarized ¹³C Metabolites

PURPOSE: To investigate the exchange and redistribution of hyperpolarized ¹³C metabolites between different pools by temporally analyzing the relative fraction of dual T₂* components of hyperpolarized ¹³C metabolites. MATERIALS AND METHODS: A dual exponential decay analysis of T₂* is performed for [1-¹³C] pyruvate and [1-¹³C] lactate using nonspatially resolved dynamic ¹³C MR spectroscopy from mice brains with tumors (n = 3) and without (n = 4) tumors. The values of shorter and longer T₂* components are explored when fitted from averaged spectrum and temporal variations of their fractions. RESULTS: The T₂* values were not significantly different between the tumor and control groups, but the fraction of longer T₂* [1-¹³C] lactate components was more than 10% in the tumor group over that of the controls (P < 0.1). The fraction of shorter T₂* components of [1-¹³C] pyruvate showed an increasing tendency while that of the [1-¹³C] lactate was decreasing over time. The slopes of the changing fraction were steeper for the tumor group than the controls, especially for lactate (P < 0.01). In both pyruvate and lactate, the fraction of the shorter T₂* component was always greater than the longer T₂* component over time. CONCLUSIONS: The exchange and redistribution of pyruvate and lactate between different pools was investigated by dual component analysis of the free induction decay signal from hyperpolarized ¹³C experiments. Tumor and control groups showed differences in their fractions rather than the values of longer and shorter T₂* components. Fraction changing dynamics may provide an aspect for extravasation and membrane transport of pyruvate and lactate, and will be useful to determine the appropriate time window for acquisition of hyperpolarized ¹³C images.

Lactate oxidation in rats after strenuous exercise / 体力科学

Oxidation of lactate at rest (RE, n=4), or after short strenuous exercise (EX, n=6) was investigated in rats. Food and water were given ad libitum before experiment. In EX, rats ran to exhaustion at the speed of 80-100 m·min<SUP>-1</SUP>. Immediately after exercise, 4 μCi of (U-<SUP>14</SUP>C) lactate was injected into aorta through an indwelling catheter. In RE, (U-<SUP>14</SUP>C) lactate was injected into the rats at rest. Expired gas was collected by a Brooks type bottomless chamber on treadmill belt for 120 min. In EX, exercise duration was 109±18 sec (mean±SE), and maximum blood lactate concentration after the exercise was 23.7±2.1 mM (mean±SE) . Cumulative percent recovery of <SUP>14</SUP>C as <SUP>14</SUP>CO<SUB>2</SUB> for 120 min was 48.5±2.8% for EX and 61.7±0.9% for RE (mean±SE) . Significant difference was found between these two rates (p<0.01) . After 50 min of recovery, mean volume of <SUP>14</SUP>CO<SUB>2</SUB> expired per min in RE was significantly greater than that in EX (p<0.01) . Mean volume of <SUP>14</SUP>CO<SUB>2</SUB> expired per min per VCO<SUB>2</SUB> in RE was always greater than that in EX, and significant difference was found at 7.5 min of recovery (p<0.01) . It is concluded that although the rate of recovery of <SUP>14</SUP>C as <SUP>14</SUP>CO<SUB>2 </SUB>after exercise is lower than that at rest, the major pathway of lactate metabolism after short strenuous exercise is oxidation.