310 E. ROBERTS AND D. G. SIMONSEN 
were not affected by ligation, and no significant histological changes were seen in 
these areas. A comparison of chromatograms of the infarcted area with a normal 
area from the ventricle of each dog showed little change in 30 min and 2h after 
ligation (Figs. 107, 108). At these periods there was marked capillary congestion 
with minimal histological changes. In the 4-h experiment (Figs. 10g, 110), in which 
slight pericarditis was noted but minimal gross abnormality of the muscle fibers in 
the section studied, there was a decrease in aspartic acid by comparison with the 
control, but otherwise there was no change in amino acid pattern. At the 8-h interval 
(Figs. 111, 112) there was a decrease in glutathione content as well as in aspartic 
acid. The contents of the other detectable constituents remained unchanged. At 
this time segmentation of the muscle fibers, necrosis, loss of cross-striations, and 
extravasation of red corpuscles and polymorphonuclear leukocytes into the infarcted 
area were noted. Further changes had occurred in the amino acid pattern at 16 h 
after ligation (Figs. 113, 114). A marked decrease in content of taurine was noted 
as well as decreases in the levels of alanine, glutamine, glutamic and aspartic 
acids, glutathione and ethanolamine phosphate. Further significant changes appeared 
to have taken place at 24 and 48h (Figs. 115-118). A sample obtained from a dog 
surviving the ligation for 5 days (Fig. 120) showed a great loss of all of the constit- 
uents in the infarct by comparison with the control area (Fig. 119). Losses of 
carnosine from the affected areas also occurred, the quantities of /-alanine and 
histidine detected on chromatograms of acid-hydrolyzed extracts being decreased 
markedly at 16 h after ligation and at later time intervals. 
From this study it is apparent that extensive damage in the heart muscle did not 
result in the immediate loss of the easily extractable ninhydrin-reactive constituents, 
but rather that this loss took place over a considerable period of time. At the time 
that marked changes in amino acid content became apparent the degree of damage 
to the myocardium was of such an extent that probably many of the cellular con- 
stituents of both higher and lower molecular weight were lost. However, not all 
injury to muscle results in the loss of amino acids. Determinations of free amino 
acids and related substances in extracts of muscle from normal and vitamin E 
deficient (dystrophic) rabbits have shown that in a severely dystrophic rabbit a 
number of the amino acids in the picric acid filtrates were elevated, but that the 
contents of glycine, histidine, 1-methylhistidine, carnosine and anserine were markedly 
reduced*. 
Free amino acids of tumors grown in resistant and susceptible hosts 
The results to be reported in this section again serve to emphasize the stability of 
those properties of cells which are related to the retention of relatively high levels 
of the easily extractable ninhydrin-reactive constituents. Tumor cells have been 
shown to have the capacity to retain much larger concentrations of the amino 
constituents than are found in extracellular fluid of the tumors even when severe 
cellular damage was produced as judged by cytological criteria. 
Determinations were made by two-dimensional paper chromatography of free 
amino acid patterns in tumor C1408 in both solid and ascites forms at various times 
after transplantation into C57BL/10-H-2’ mice, a strain in which the tumor grows 
progressively and kills the animals, and into C57BL/10-H-2% mice, a subline which 
References p. 348/349 
