CHANGES OF FIBRONECTIN IN THE RIGHT-AND-LEFT-VENTRICLES OF RATS EXPOSED TO CHRONIC NORMOBARIC HYPOXIA

Changes of fibronectin (FN) in the right and left ventricles of adult rats exposed to chronic normobaric hypoxia were observed by a peroxida se immunohistochemical stain technique and analyzed quantitatively by a point counting method. Fifty-six rats were randomly divided into con trol groups of day 0 (immediately prior to the experiment), day 5, day 15, and day 30 and hypoxia groups of day 5, day 15, and day 30. Rats of the hypoxia groups were put into a normobaric hypoxia chamber with oxygen concentration adjusted to 10 percent. The rats of the control g roups breathed room air. From day 5 on, the ratio of the weight of the right ventricle (RV) to that of the left ventricle (LV) plus interven tricular septum (SP), RV/(LV + SP), and the ratio of the weight of the right ventricle (RV) to the body weight (BW), RV/BW, in the hypoxia g roups increased significantly as compared with those of the control gr oups. The amount of immunoreactive FN in the right ventricle increased significantly in the hypoxia groups after exposure to hypoxia environ ment for 15 days (10.31% +/- 2.15%, mean +/- S.D.) and for 30 days (9. 55% +/- 1.65%) as compared with those in the day 0 control group (3.05 % +/- 1.15%, p < 0.01), the day 15 control group (3.26% +/- 0.83%, p < 0.01), and the day 30 control group (3.19% +/- 0.51%, p < 0.01). Howe ver, there were no significant changes in the amount of immunoreactive FN in the left ventricle of the hypoxia groups as compared with the c ontrol groups. These results suggest that chronic hypoxia may lead to an increase of FN in the hypertrophied right ventricle but not in the left ventricle, which indicates that pulmonary hypertension induced by chronic hypoxia rather than chronic hypoxia itself is a major cause f or the increase of FN in the myocardium. The increased FN in the right ventricle may accelerate the accumulation of collagen and, in turn, c ontribute to the increase of the myocardial stiffness and eventually t o the diastolic dysfunction of the hypertrophied right ventricle induc ed by chronic hypoxia.