272 
PULMONARY MODELS 
activity, or a diminished response to acute hy- 
poxia. The lack of hyperventilation most cer- 
tainly contributes to the pulmonary hyperten- 
sion and provides a good model of pulmonary 
hypertension without lung disease. 
3. Excision of the carotid bodies in calves re- 
sults in marked hypoventilation, in increase in 
PaCOo, a decrease in Pa02, and the develop- 
ment of pulmonary hypertension at a moderate 
altitude (1,600 m), thus providing a model of 
chronic respiratory acidosis and cor pulmonale 
in the absence of airway disease. 
4. Although the regional distribution of ven- 
tilation and perfusion in the bovine lung is dif- 
ferent from man, and perfusion apparently is 
not totally dependent upon gravity for its dis- 
tribution, nevertheless, the calf remains a valu- 
able animal to study the mechanisms which 
influence the relationship of blood flow to ventila- 
tion under a variety of conditions. 
REFERENCES 
1. Tucker, C. E., Will, J. A., and Grover, R. F. 
Pulmonary hypertension in the goat at high alti- 
tude. The Physiologist 12:378, 1969. 
2. Banchero, N., Grover, R. F., and Will, J. A. 
High altitude-induced pulmonary hypertension in 
the llama (Lama glama). Amer. J. Physiol. 
220:422-427, 1971. 
3. Grover, R. F., Reeves, J. T., Will, D. H., and 
Blount, S. G., Jr. Pulmonary vasoconstriction in 
steers at high altitude. J. Appl. Physiol. 
18:567-574, 1963. 
4. Hecht, H. H., Kuida, H., Lange, R. L., Thorne, 
J. L., and Brovs^n, A. M. Brisket disease II. Clini- 
cal features and hemodynamic observations in alti- 
tude-dependent right heart failure of cattle. Amer. 
J. Med. 32:171-183, 1962. 
5. KiRSH, M. M., Kahn, D. R., Lucchesi, B., Gago, 
O., Dufek, J. H., Lee, R. W. S., Stutz, D., and 
Sloan, H. Effect of glucagon on pulmonary vascu- 
lar resistance. Surg. 70:439-442, 1971. 
6. Byrne-Quinn, E., and Grover, R. F. Aminorex 
(MenociP) and amphetamine: Acute and chronic 
effects on pulmonary and systemic haemodynamics 
in the calf. Thorax 1972 (In Press). 
7. Ruiz, A. V. Cardiopulmonary function in calves 
during acute hypoxia and hyperoxia at sea level 
and altitude. Ph.D. Thesis, University of Wiscon- 
sin, 1972. 
8. BiSGARD, G. E., and Vogel, J. H. K. Hypoven- 
tilation and pulmonary hypertension in calves af- 
ter carotid body excision. J. Appl. Physiol. 31:431- 
437, 1971. 
9. BiSGARD, G. E. Ventilatory control in the Hereford I 
calf at sea level and at 3400 m altitude. Ph.D. The- 
sis, University of Wisconsin, 1971. 
10. CoMROE, J. R., Forster, R. E., II, Dubois, A. B., 
Briscoe, W. A., and Carlson, E. The Lung, Clin- I 
ical Physiology and Pulmonary Function Tests. \ 
2nd ed., Chicago. Yearbook Medical Publishers, i 
Inc., 1965. 1 
11. Grover, R. F. Effects of hypoxia on ventilation | 
and cardiac output. Ann. N.Y. Acad. Sci. 
121:662-673, 1965. 
DISCUSSION 
J. R. Gillespie, University of California, 
Davis: Was the difference in the distribution 
and profusion in the calves about a 20 cm gra- 
dient? 
Dr. Will: No, that is not centimeters, Dr. j 
Gillespie, that's based on per cent of total lung J 
profusion. ' 
Dr. Gillespie : Yes, I understand that, but I | 
meant what is your total gradient? About 20 ' 
cm? 
Dr. Will : No, it's a little more than that on 
these calves. I would say it's more in the neigh- , 
borhood of 30 cm. 
Dr. Gillespie: What I'm wondering is, did 
you tilt the calf in any other position to see if 
redistribution occurred? , 
Dr. Will: No, we did not. However, we just I 
finished eleven human subjects at Leadville two j 
weeks ago, and the gradient was narrower in | 
man than it was in the calves that we studied, j 
so we don't feel that the gradient between the j 
top and the bottom of the lung would be a fac- ■ 
tor in this. 
Gerald Moss, Rennselaer Polytechnic Insti- 
tute, Troy, N.Y. : You mentioned that the calf's <■ 
arterial oxygen saturation does actually go ; 
down when he goes to altitude. Yet, I was sur- i 
prised that the venous oxygen saturation didn't 
show a compensatory decrease also. So, it looks 
as if there is less of an A-V gradient. ■ 
Dr. Will : That's right. 
Dr. Moss : Which means, if the animal is me- 
tabolizing normally, his cardiac output must be | 
going up. I wonder if there's any measurement | 
there, whether this may be contributing to the I 
failure? I'm just wondering how much of an in- ] 
crease in cardiac output you have because of ^ 
this hypoxemia? 
