194 
PULMONARY MODELS 
neous clinical recovery in approximately 50% 
of the cases. 
Pathologically, affected animals have lesions 
of generalized passive congestion with edema, 
hydrothorax, ascites, and cor pidmonale. Post 
mortem pulmonary arteriography has demon- 
strated deai'borization of the pulmonary ar- 
terial tree/' indicative of an increased precapil- 
lary resistance to flow. Light microscopic 
examination of the lungs has revealed medial 
smooth muscle hypertrophy and adventitial pro- 
liferation around the small pulmonary arteries 
and arterioles.'' '^ Distal occlusion of small arter- 
ies by thrombi, emoli, or intimal proliferation is 
not present, nor has morphological evidence of 
postcapillary obstruction been recognized. 
METHODS 
Experimental studies have demonstrated that 
normal cattle taken from a low to a high alti- 
tude develop significant pulmonary hyper- 
tension. Increasing the test altitude hastens 
the development of pulmonary hypertension, 
indicative of the apparent marked sen- 
sitivity of the bovine pulmonary vasculature to 
changes in oxygen tension.^ The effect of simu- 
lated altitudes in a hypobaric chamber of 15,000 
and 20,000 feet on eight calves is shown in Fig- 
ure 1. The time course for the development of 
severe pulmonary hypertension and congestive 
failure was shorter for the animals at 20,000 
feet. Likewise, the time required to develop se- 
Day* at high altitud* 
Figure 1. — Effect in cattle of 15,000 and 20,000 feet 
altitude (hypooarie chamber) on pulmonary vascular 
pressure. 
vere pulmonary hypertension at 15,000 feet was 
slightly less than at 12,700 feet,^ which in turn 
was less than at 10,000 feet.^ In general, in the 
absence of significant increases in flow, blood 
viscosity, and pulmonary arterial wedge pres- 
sures, the pulmonary hypertension has been at- 
tributed to a decrease in the cross sectional area 
of the pulmonary vascular bed at the precapil- 
lary level. 
The magnitude of the pulmonary hyperten- 
sion, which develops when cattle are moved to 
high altitudes shows considerable variation. 
Some animals develop only moderate pulmonary 
hypertension, while others develop severe hyper- 
tension leading to congestive right heart fail- 
ure.®'' None of the functional or morphological 
measurements have served to clearly explain the 
marked individual differences in the response of 
cattle to high altitude. 
In a study of cattle native to and resident at 
5,000, 8,500, and 10,000 feet altitude," only low 
to moderate pulmonary hypertension was ob- 
served in the animals at the higher altitude 
(Table I). It is probable that both natural and 
artificial selection have occurred at high alti- 
tude to produce a native cattle population with 
a more hyporeactive pulmonary vascular bed 
and a low incidence of high mountain disease. 
This selection process may have tended to elimi- 
nate the hyperreactive type of animal. 
Many unpublished statements, implications, 
and observations have been made that strongly 
indicate that the susceptibility of cattle to high 
mountain disease may be partially but signifi- 
cantly heritable. Although difficult to prove on 
an epidemiologic study basis, certain breeds ap- 
pear to have greater susceptibility to the spon- 
Table L — Mean Pulmonary Arterial Pressures in Cattle 
Resident at Different Altitudes 
Resident Altitude in Feet 
Age 
5.000 
8,500 
10,000 
4-8 years 
Number 
4 
IB 
17 
Mean PAP* 
29.8 
38.2 
37.4 
Std. Dev. 
2.5 
6.4 
7.9 
2 years 
Number 
10 
16 
30 
Mean PAP 
30.1 
28.5 
27.7 
Std. Dev. 
4.3 
4.6 
9.8 
4-6 months 
Number 
10 
15 
17 
Mean PAP 
30.1 
28.5 
37.7 
Std. Dev. 
2.3 
4.8 
16.8 
* Pulmonary arterial pressure, mm Hg. 
