A. F. ALEXANDER, C. S. CARD, R. S. JAENKE, J. L. HICKS, AND D. H. WILL 
199 
Figure 8. — Arteriole at level of terminal bronchiole 
from a normotensive animal. Media comprised of 
thin single layered smooth muscle. Epon section; 
Richardson stain X 425. 
The light microscopic alterations of pulmon- 
ary hypertensive vascular disease have been 
described in considerable detail. i" -" Many stud- 
ies, however, have been concerned with hyperki- 
netic states in which the pulmonary blood flow 
is increased. Although the vascular lesions of 
hypoxic pulmonary hypertension show some 
similarity to these high pressure/high flow sys- 
tems, the end stages of vascular necrosis, severe 
intimal proliferation, and plexiform forma- 
tions, are seldom observed. Essentially, the hy- 
poxic induced vascular lesions are characterized 
by marked medial thickening (Figures 8 and 
9), moderate intimal proliferation in larger ar- 
teries and adventitial proliferation,^'^'2i,22 
A number of reports have dealt with the cel- 
lular pathology of systemic hypertension.^^-ss 
Our own ultrastructural investigations of small 
pulmonary arterial vessels in hypoxic-indueed 
pulmonary hypertension have revealed basic 
similarities to the hypertensive lesions of sys- 
temic arterioles.2^ Fine structural studies pro- 
vide evidence for cellular degenerative changes. 
A more important alteration maybe a change in 
the basic metabolic function of the medial 
smooth muscle cells as well as the endothelium, 
evidenced by changes in morphologic patterns 
of the subcellular organelle systems. Further in- 
vestigations are being conducted in an attempt 
to relate these morphological changes to basic 
functional changes in hypertensive vessels. 
SUMMARY 
The marked reactivity of the bovine pulmon- 
ary vascular bed to chronic inhalation hypoxia 
make this species of distinct value as a model 
for studies of hypoxic-indueed pulmonary hy- 
pertension. Variations in the levels of pulmon- 
ary hypertension and vascular resistance ob- 
served between individual cattle will probably 
ultimately be defined in functional and morpho- 
logical terms. However, heredity appears to play 
a prominent role in governing these factors and 
should be considered in the interpretation of ex- 
perimental results. 
REFERENCES 
1. Will, D. H., and Alexander, A. F. High moun- 
tain disease. In Bovine Medicine and Surgery, 1st 
ed. Am. Vet. Publications, Inc., Wheaton, Illinois, 
1970. 
2. Hecht, H. H., Kuida, H., Lange, R. L., Thorne, 
J. L., and Brown, A. M. Brisket disease II Clini- 
cal features and hemodynamic observations in alti- 
tude-dependent right heart failure in cattle. Amer. 
J. Med. 32:171-183, 1962. 
3. Glover, G. H., and Newsom, I. E. Brisket dis- 
ease. Colorado Agric. Expt. Sta. Bull. 204, 1915. 
4. Vogel, J. H. K., McNamara, D. G., Hallman, 
G., Rosenberg, H., Jamieson, G., and McGrady, 
Figure 9. — Arteriole with small lateral branch at level 
of terminal bronchiole from a hypertensive animal. 
Note thickened media with prominent overlapping 
smooth muscle cells; decreased luminal size and ap- 
parent adventitial proliferation. Epon section; Rich- 
ardson stain X 425. 
