• 1 January 1980
    • journal article
    • research article
    • Vol. 42  (6) , 603-615
Abstract
Hypoxia is known to cause an increase in thickness of the medial and adventitial layers of the muscular pulmonary arteries, but little is known of its effect on the endothelial cell and the rest of the intima. The ultrastructural changes in the intima of the hilar intrapulmonary muscular artery of the rat after exposure to hypobaric hypoxia of 380 torr for 10 days and their resolution during recovery periods of between 3 and 70 days in room air are described. After 10 days of hypoxia, the intima is 3 times thicker than the controls (control = 1.81 .mu.m .+-. 0.13 SE; hypoxia = 5.59 .mu.m .+-. 1.14 SE; P < 0.05). The thickness of the endothelial cell layer doubles (control = 1.57 .+-. 0.12 SE; hypoxia = 3.29 .mu.m .+-. 0.23 SE; P < 0.001) and point-counting the cytoplasm of these cells reveal significant relative increase in areal proportions and most marked hypertrophy, of ribosomes, rough endoplasmic reticulum and Golgi apparatus. An increase in number of endothelial cells is apparent. The increase in thickness of the subendothelial layer is due to appearance of edema. Microfibrillar basement membrane-like material is found focally within the subendothelial layer. In some sections .apprx. 50% of the endothelial associated basement membrane is absent. During recovery periods, there is regression of all the hypoxia-induced changes, except that the amount of subendothelial elastin increases to day 28 recovery, thereby altering the structure of the wall. The presence of elastin, collagen fibers and microfibrils on the luminal side of the endothelial basement membrane in control and experimental animals points to their synthesis by the endothelial cell. [Hypoxia-induced pulmonary hypertension is associated with an increase in medial and adventitial thickness of the normally muscular pulmonary arteries.].