• 1 January 1980
    • journal article
    • research article
    • Vol. 100  (1) , 151-178
Abstract
Chronic hypobaric hypoxia induces structural features characteristic of pulmonary hypertension, but little is known of their reversal. Rats were exposed to hypobaric hypoxia for 10 days and subsequently allowed to recover in room air for 3, 14, 28 or 70 days. With the use of 1 .mu. sections and EM and point-counting techniques, the regression of the medial and adventitial changes in the rat hilar intrapulmonary artery was followed. In the media 10 day hypoxia caused more than a doubling in thickness due to hypertrophy of smooth muscle cells [particularly of rough sarcoplasmic reticulum and Golgi apparatus], an increase in extracellular connective tissue, microfibrils, collagen fibers and elastin, and edemalike fluid. Elastic laminas were doubled in thickness, and myofilamentous processes of the hypertrophied smooth muscle cells contacted them. After just 3 days'' recovery, some cells already returned to normal diameter, although medial thickening was unchanged. By day 14 and at days 28 and 70 of recovery medial thickness and cell diameter are within the normal range, and by recovery day 70 there is a significant increase in the relative areal proportion of extracellular collagen fibers and a decrease in elastin (P < 0.001). Hypoxia produced a more than two-fold increase in adventitial thickness. Hypertrophy of fibroblasts and an increase in their number contributed to the thickening, as did an increase in collagen fibers. During 3-70 days of recovery thickness gradually reduced to normal levels, although it was still significantly above normal at days 3, 14 and 28. The increases in thickness at these times were due mainly to the accumulation of collagen fibers, which were still apparent after 70 days of recovery. Hypoxia causes a doubling in thickness of the medial and adventitial coats of the hilar muscular pulmonary artery, which with recovery regain near-normal thickness but whose structure was altered. The increase in collagen fibers contributes to contracture and reduced distensibility in these vessels. This is apparent in arteriograms as narrowed lumen diameter.