R. A. KAINER, C. S. CARD, AND G. P. EPLING 
219 
1-tryptophan per kg of body weight was given, 
and, once again, clinical signs were not ap- 
i parent. However, her pulmonary arterial pres- 
sure doubled 72 hours after treatment and then 
decreased to normal pressure by 120 hours. She 
was not slaughtered at that time. 
This marked increase in pulmonary arterial 
pressure was noted in two other cows. In a six- 
year-old Hereford (A201, Table I) there were 
no clinical signs following a dose of 0.7 g 
1-tryptophan per kilogram of body weight, but 
her pulmonary arterial pressure doubled on the 
fourth and fifth days after treatment. At post- 
mortem examination following immobilization 
with succinylcholine chloride gross pulmonary 
lesions were equivocal. Mild lesions were ob- 
served in microscopic sections from the right 
diaphragmatic lobe. Epithelial proliferation 
without attendant inflammatory changes was 
observed at the light microscopic level. Under 
the electron microscope the proliferated cells 
resembled bronchiolar epithelial cells more 
closely than pneumonocytes (Figure 1). In sur- 
faces not covered by these cells degeneration of 
the blood-air barrier was observed (Figure 2). 
A very old, weak Hereford cow (480, Table 
I) had a hypertensive pulmonary arterial 
Figure 1. — Electron micrograph of a proliferated cell 
lining an alveolus. Orig. mag. 4300 X- 
pressure (70 mm Hg) prior to treatment. It 
increased 1.6 times (to 115 mm Hg) 24 hours 
following the administration of 0.525 g 1-try- 
ptophan per kilogram of body weight. She was 
down in right lateral recumbency in the corral 
on the second day, and her pulmonary arterial 
pressure was not recorded. On the third day 
her pulmonary arterial pressure was slightly 
below the pretreatment level. At postmortem ex- 
amination following euthanasia there was 
chronic suppurative pneumonia in the ventral 
one-third of all lobes of the left lung with strong 
adhesions to the parietal pleura. The gross ap- 
pearance of the right lung was normal. Signifi- 
cant pulmonary lesions were lacking in micro- 
scopic sections from this lung. 
DISCUSSION 
In our hands the intraruminal administration 
of d,l- or 1-tryptophan did not induce clinical 
signs resembling those ascribed to acute bovine 
pulmonary emphysema. Johnson and Dyer^ re- 
ported that five out of eight cattle died follow- 
ing the oral administration of d, 1-tryptophan. 
Dickinson et al.* described clinical signs of 
respiratory distress and pulmonary lesions 
varying from mild to severe in seven to eight 
cows receiving oral d,l-tryptophan. Seven cows 
given oral doses of this amino acid by Carlson 
et al.io developed typical signs of interstitial 
pulmonary emphysema. Four of these cows died 
in 11/2 to 41/2 days following tryptophan admin- 
istration. The conditions of our experiments 
were based on those described in the papers 
cited above.*'"'^^ 
One can speculate on nutritive variations in 
the grass hay fed in these geographically sepa- 
rated experiments; there are no definite data 
on such differences. Three old cows in poor 
physical condition were selected on the premise 
that they would be more likely to have had pre- 
vious pulmonary insults. Even with this experi- 
mental bias, clinically observable signs of acute 
pulmonary emphysema could not be provoked 
by the administration of tryptophan. If pre- 
vious pulmonary pathology were invariably pre- 
disposing, then the old, debilitated Hereford 
cow with chronic suppurative pneumonia should 
have responded with clinical signs of acute res- 
