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Journal of Applied Physiology, Vol 55, Issue 5 1445-1455, Copyright © 1983 by American Physiological Society
ARTICLES |
S. S. Sobin, H. M. Tremer, J. D. Hardy and H. P. Chiodi
After 1 h of exposure to 0.5 atm of pressure, the electron microscopy of intra-acinar arterioles of the young female adult rat showed edema and subendothelial blebs. Pulmonary hypertension developed rapidly with an increase in hemoglobin, hematocrit, and right ventricular weight. By 24 h, there was a threefold increase in the number of fibroblasts within the arteriolar wall, followed during the next 2 days by transformation of the fibroblast through a transitional cell form to a smooth muscle cell. By 1 wk, the neomuscularization was essentially complete. There was further minor thickening and increase in density of the wall over the next 9 mo. On return to 1 atm after prolonged hypoxia, within 4 wk, the smooth muscle of neomuscularized arterioles dedifferentiated but did not disappear. There was a concurrent rapid fall in the pulmonary arterial pressure, hemoglobin, hematocrit, and right ventricular weight. Veins, capillaries, and arteries remained normal. Parallel studies in the male rat during 14 days of hypoxia demonstrated the same phenomena except slightly accelerated over the female. The rapid sequential changes in the arteriole, beginning with subendothelial blebs and wall edema, followed by fibroblast recruitment and transformation into smooth muscle through a transitional cell form, suggest a cascade. The anatomic and physiological responses to hypoxia are not sex related.
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