Journal of Applied Physiology, Vol 67, Issue 4 1383-1387, Copyright © 1989 by American Physiological Society
Chronic CO exposure stimulates erythropoiesis but not glomus cell growth
A. K. Sherpa, K. H. Albertine, D. G. Penney, B. Thompkins and S. Lahiri
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104-6085.
The effect of chronic CO exposure, which stimulates erythropoietin
production and erythropoiesis, was studied on carotid body cells in the
rat. The hypothesis to be tested was that chronic CO inhalation would
stimulate cellular hypertrophy and hyperplasia of carotid body if it caused
local tissue hypoxia as in chronic hypoxia. The failure of an appropriate
response would indicate a lack of a specific local effect on carotid body
tissue PO2 presumably because of its unusually high tissue blood flow. Six
young male rats were exposed to 0.4-0.5 Torr (0.05-0.07%) inspired PCO in
air for 22 days. Control rats (n = 6) were maintained under similar
conditions except for CO exposure. After the exposure period the rats were
anesthetized, blood was collected for hematocrit, and the carotid bodies
were surgically exposed and fixed for electron microscopy and morphometry
of type I and type II cells and capillary endothelium. Hematocrit was
significantly greater in the CO-exposed group (75 vs. 48%), whereas no
significant difference was found in the carotid body parenchyma between the
control and CO-exposed groups. We conclude that the lack of an effect of
chronic CO exposure on the carotid bodies in contrast to the strong
erythropoietic response indicates a relatively high tissue blood flow rate
in the carotid body and that CO did not exert a direct cellular effect. The
results also suggest that the hypertrophic response of carotid body glomus
cells to chronic hypoxic hypoxia is the result of a local direct effect of
low PO2 rather than secondary to systemic effects.
