Changes of pulmonary tissue area density and their mechanisms in rats with hypoxic pulmonary hypertension.
- Author:
Sheng-xian WANG
1
;
Zhong-he YU
;
Ying ZHOU
;
Min-qin ZHENG
;
Li GONG
;
Yi JIAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Hypertension, Pulmonary; etiology; pathology; physiopathology; Hypoxia; physiopathology; Lung; pathology; ultrastructure; Male; Microscopy, Electron; Random Allocation; Rats; Rats, Wistar
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2003;21(5):350-352
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the changes of pulmonary tissue area density and their mechanisms in rats with hypoxic pulmonary hypertension (HPH).
METHODS54 Wistar rats were divided into hypoxia 10 d (n = 12), 20 d (n = 12), 30 d (n = 12) groups and control group (n = 18). The rats in hypoxia groups were exposed to a simulated hypoxia environment at a height of 5 km above sea level to establish HPH models. The changes in pulmonary tissue area density and pathological morphology were determined by image analysis, optical microscope, electron microscope and histochemistry.
RESULTSAfter hypoxia, the pulmonary tissue area density markedly increased on 10 d (27.08% +/- 1.29%, P < 0.05), especially on 20 d (31.33% +/- 0.27%) and 30 d (31.10% +/- 1.95%) while that in control group was 22.78% +/- 1.17% (P < 0.01). The area density on 20 d was higher than that on 10 d (P < 0.05) but there wasn't significantly different between 10 d and 30 d (P = 0.057) after hypoxia. Pathological examination showed: edema and collapse of pulmonary tissue, swelling and degeneration of type II alveolus epithelial cells (PII); congestion, accumulation of polymorphonuclear neutrophils and platelets in capillaries; swelling and degeneration of endothelial cells, thickening of basement membranes.
CONCLUSIONSHypoxia can induce increase in pulmonary tissue area density and decrease in aerial exchange area in alveoli. These changes may be related to the pulmonary collapse caused by the damage of PII and pulmonary surfactant system, structural remodeling of small pulmonary arteries, increase in blood cells and protein granules in alveolar cavity.