ACUTE BOVINE PULMONARY EMPHYSEMA: 
EVALUATION OF TRYPTOPHAN INDUCTION 
R. A. Kainer, C. S. Card and G. P. Epiing* 
Consistent ultrastructural changes occur at the blood- 
air barrier during the initial stages of the poorly-de- 
fined disease complex, acute bovine pulmonary emphy- 
sema. Intracellular edema, organellar degeneration and 
rupture of the plasma membrane in the mebranous 
pneumonocyte is followed by the same sequence of events 
in the endothelial cell and, finally, by degeneration and 
disruption of the basal laminae of these cells. Nine at- 
tempts were made to induce this disease complex under 
controlled conditions in order that pathophysiologic 
parameters could be correlated with morphologic 
changes. Eight cows (6 Herefords, 1 Brown Swiss- 
Jersey crossbred and 1 Holstein-Friesian) varying in 
age from 5 to 15+ years and varying in physical con- 
dition from excellent to poor were used in these trials. 
Intraruminal administration of 0.7 g d,l-tryptophan per 
kg of body weight or 0.35 g, 0.525 g or 0.7 g of 1-tryp- 
tophan per kg of body weight failed to induce clinical 
signs of acute bovine pulmonary emphysema in any of 
the cows. Cardiovascular, pulmonary and hematologic 
parameters remained unchanged with the exception of 
three instances in which there was a marked but transi- 
tory elevation of pulmonary arterial pressure one to 
four days following the administration of tryptophan. 
In one of these three cows alveolar septal degeneration 
and epithelial proliferation were observed in micro- 
scopic sections from a diaphragmatic lobe. It was sug- 
gested from the ultrastructural cytology of the pro- 
liferated cells that they were derived from bronchiolar 
epithelium. 
INTRODUCTION 
An animal afflicted with acute bovine pul- 
monary emphysema is typically a middle-aged, 
lactating cow which has been moved from a dry, 
late summer pasture to a lush, green, usually 
irrigated pasture.^^-^ Within a few days she 
becomes severely dyspneic with her head ex- 
tended and her breathing characterized by a 
forced expiratory effort. The course of the dis- 
ease is rapid, and the mortality is high. 
The descriptive term, acute bovine pulmonary 
emphysema, is considered a misnomer by many, 
since the progressive lesions are not those estab- 
* College of Veterinary Medicine & Biomedical Sciences, Colorado 
State University, Fort Collins, Colorado. 
lished for chronic pulmonary emphysema in 
man. Synonyms such as cow asthma, panting 
disease, atypical interstitial pneumonia and pul- 
monary adenomatosis also are not completely 
accurate descriptions of this syndrome. Not- 
withstanding semantics and the vagaries of 
comparative pathology, different investiga- 
tors have described alveolar expansion, thin- 
ning and some rupture of alveolar walls, and 
focal hemorrhage. There is little or no exudative 
obstruction, but there is a strong suggestion 
of bronchiolar constriction. Pulmonary edema 
is seen commonly, and, as the disease pro- 
gresses, there is an invasion by macrophages, 
plasma cells and, occasionally, granular leuko- 
cytes. Interstitial fibrosis is not pronounced. 
However, there is an intra-alveolar prolifera- 
tion of epithelium which has been described as 
alveolar epithelium ^ but which may be of bron- 
chiolar origin. Marked interstitial emphysema 
is a complication seen at necropsy in the dis- 
tended, uncollapsed lungs. 
A SEQUENCE OF ALVEOLAR DESTRUCTION 
Epiing, who earlier described the ultrastruc- 
ture of the blood-air barrier in the bovine lung,® 
has elucidated the sequences of ultrastructural 
change in the thinning alveolar septa. A uni- 
form sequence of degeneration of the alveolar 
wall was observed in regions where there was 
some alveolar hemorrhage. 
Intracellular edema occurred first in mem- 
branous pneumonocytes. There was gradual re- 
duction of micropinocytotic vesicles, enlarge- 
ment of the cisterns of endoplasmic reticulum, 
mitochondrial swelling, expansion of the cyto- 
plasmic matrix, and, finally, rupture of the 
plasma membrane which exposed the alveolar 
basal lamina to the lumen of the alveolus. This 
sequence then took place in the same manner 
within the pulmonary capillary endothelial 
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