444 G. ROUSER et al. 
in the cells following ingestion of this amino acid than in the control samples. The 
high degree of reproducibility of the erythrocyte free amino acid pool after glutamine 
ingestion is illustrated in Figs. 340-349. 
Figs. 350-362 show the free amino acid pools of the lymphocytes from subject 
R. Tho. The control samples in Figs. 350-352 are similar. The glutamine level in the 
leukocytes rose to reach a peak at 85 min (Fig. 356) that was maintained through 
the 175-min sample (Fig. 358). The level then fell to the level observed in control 
samples. The elevation of glutamine in the leukocytes of this subject was somewhat 
less than the elevation observed for granulocytes described below. 
Each individual urine specimen from subject R. Tho. for 24 h before the glutamine 
ingestion study, all specimens obtained during the day of the study, and all specimens 
collected for 24h after the study were kept separately and examined by paper 
chromatography (a total of 15 specimens). The free amino acid levels of the urine 
(not illustrated) were very uniform and the results were in keeping with those of 
the hematologically normal individuals in that no change in glutamine or other free 
amino acids was noted following the ingestion of glutamine. 
Glutamine ingestion in chronic granulocytic leukemia 
Patient H. Gol. (chronic granulocytic leukemia) without any previous form of treatment 
and a white cell count of 450 000/mm? was studied as follows. Three control blood 
samples were drawn. 50g of glutamine was consumed in 400 ml of water over a 
period of 10 min, and additional blood samples were drawn 15, 35, 60, 90, 120, 150, 
180, 250, and 305 min after ingestion of glutamine. 
Figs. 363-372 show the plasma samples from patient H. Gol. Only the second of 
the three control samples is shown (Fig. 363). The three control samples are presented 
in part I of this series (Figs. 32-34, p. 362) to illustrate the marked venipuncture res- 
ponse. The plasma glutamic acid levels of the control samples were far above the 
levels encountered in normal individuals (compare Fig. 363 with Figs. 268, p. 431 and 
304, p. 437) and most patients with chronic lymphatic leukemia (compare Fig. 363 with 
Figs. 324-3260, p. 439). A definite elevation of the levels of most of the other amino 
acids can be observed also (see the complete discussion of the findings in chronic 
granulocytic leukemia in part IT). 
Following the ingestion of glutamine, the glutamic acid level rose to a peak at 
about 60 min and fell to below control levels at the end of the study. The level of 
the uncharacterized substance migrating just to the left of glutamic acid on chro- 
matograms also rose and fell. The peak glutamine level was maintained through 
120 min. The rise in plasma glutamine was not as marked as that observed in the 
three hematologically normal individuals or the patient with chronic lymphatic 
leukemia. 
The glutamine levels of erythrocytes and leukocytes from subject H. Gol. (not 
illustrated) rose slightly and then returned to control levels. 
Two other granulocytic leukemia patients without any previous form of treatment 
were studied in the same manner as for the other subjects. Each ingested 50 g of 
glutamine and control and experimental samples were drawn at intervals similar to 
the ones above. The samples were examined by paper chromatography and glutamine 
was assayed with glutaminase. Fig. 377 shows the glutamine levels determined by 
enzymatic assay in the plasma, erythrocytes, and leukocytes of subject Q. Tur., and 
References p. 447/448 
