Xu Y, Shiraishi K, Mori M, Motomiya M
Internal Department of Tongji Hospital, Tongji Medical University, Wuhan, People's Republic of China.
Tohoku J Exp Med. 1992 Dec;168(4):573-82. doi: 10.1620/tjem.168.573.
Changes of fibronectin (FN) in the right and left ventricles of adult rats exposed to chronic normobaric hypoxia were observed by a peroxidase immunohistochemical stain technique and analyzed quantitatively by a point counting method. Fifty-six rats were randomly divided into control 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 groups 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 interventricular 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 groups increased significantly as compared with those of the control groups. The amount of immunoreactive FN in the right ventricle increased significantly in the hypoxia groups after exposure to hypoxia environment 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). However, there were no significant changes in the amount of immunoreactive FN in the left ventricle of the hypoxia groups as compared with the control 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 for the increase of FN in the myocardium. The increased FN in the right ventricle may accelerate the accumulation of collagen and, in turn, contribute to the increase of the myocardial stiffness and eventually to the diastolic dysfunction of the hypertrophied right ventricle induced by chronic hypoxia.
采用过氧化物酶免疫组织化学染色技术观察成年大鼠在慢性常压缺氧条件下左右心室中纤连蛋白（FN）的变化，并采用点计数法进行定量分析。56只大鼠随机分为实验第0天（实验前即刻）、第5天、第15天和第30天的对照组，以及第5天、第15天和第30天的缺氧组。缺氧组大鼠置于常压缺氧舱中，将氧气浓度调至10%。对照组大鼠呼吸室内空气。从第5天起，缺氧组右心室重量（RV）与左心室加室间隔重量（LV + SP）之比，即RV/(LV + SP)，以及右心室重量（RV）与体重（BW）之比，即RV/BW，与对照组相比显著增加。缺氧组在暴露于缺氧环境15天（10.31% ± 2.15%，均值 ± 标准差）和30天（9.55% ± 1.65%）后，右心室中免疫反应性FN的含量与实验第0天对照组（3.05% ± 1.15%，p < 0.01）、第15天对照组（3.26% ± 0.83%，p < 0.01）和第30天对照组（3.19% ± 0.51%，p < 0.01）相比显著增加。然而，缺氧组左心室中免疫反应性FN的含量与对照组相比无显著变化。这些结果表明，慢性缺氧可能导致肥厚的右心室中FN增加，而左心室中未增加，这表明慢性缺氧诱导的肺动脉高压而非慢性缺氧本身是心肌中FN增加的主要原因。右心室中增加的FN可能加速胶原蛋白的积累，进而导致心肌僵硬度增加，并最终导致慢性缺氧诱导的肥厚右心室舒张功能障碍。
Zotero 插件