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Whether or not the pericytes exist in the intra-acinar pulmonary arteries and their normal structure and morphological changes during development of the structural remodeling of pulmonary vessels were observed using a pulmonary hypertension model in rats induced by monocrotaline injection. The results showed that the pericytes in the peripheral pulmonary vessels proliferated and transformed into smooth muscle cells during development of pulmonary hypertension, and at the same time, the pericytes could synthesize and secrete extracellular matrix including collagen, suggesting that the pericytes play an important role in the development of pulmonary hypertension and structural remodeling of the pulmonary vessels.

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The pulmonary arteriole remodeling in Wistar rats with respiratory infection induced by mycoplasma pneumoniae was observed using light microscopy and morphometry. The pulmonary artery pressure (PAP) and index of right ventricular hypertrophy (RVHI) were measured. The intimal and medial hypertrophy can be seen in the pulmonary arterioles, leading to vessel wall thickening and narrowing of the lumina. The total number of the pulmonary arterioles decreased (P < 0.01), and both pulmonary hypertension (Ppa 4.11 +/- 0.19 kPa) and right ventricular hypertrophy (RVHI = 34.96 +/- 3.91%) occurred. In addition, an interstitial pulmonary fibrosis (IPF) was found, in which the content of collagen in the lung tissue changed, i. e., type I collagen increased whereas type III one decreased, and the ratio of type I collagen to type III one increased. It suggested that respiratory infection induced by repeated MP may result in remodeling of pulmonary arterioles and are closely related to pulmonary hypertension.

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The inhibitory effect of Radix Salviae Miltiorrhizae (RSM) on hypoxic structural remodeling of intra-acinar pulmonary arteries (IAPA) was observed by light and electron microscopy and morphometry. It was found that RSM can not only dilate IAPA and relieve the hypoxic injuries to endothelia cells, but also inhibit the active muscularization of IAPA in the hypoxic animals, suggesting that RSM plays a very important role in inhibiting structural remodeling of IAPA and pulmonary hypertension.

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The direct effect of hypoxia and the effect of hypoxic endothelial cells conditioned medium on cultured pulmonary arterial smooth muscle cells in vitro were studied with phase contrast in microscopy, 3H-thymidine labelled technique and flow cytometric measurements. The results showed that direct hypoxia inhibited proliferation of pulmonary arterial smooth muscle cells, retained pulmonary arterial smooth muscle cells in the Go/G1 phase and decreased 3H-thymidine incorporation into pulmonary arterial smooth muscle cells and that hypoxic endothelial cells conditioned medium stimulated proliferation of pulmonary arterial smooth muscle cells, promoted pulmonary arterial smooth muscle cells from G0/G1 phase to S phase and increased 3H-thymidine incorporation into pulmonary arterial smooth muscle cells. It was reasonable to believe that hypoxia might enable pulmonary arterial endothelial cells to secrete some growth factors which could stimulate proliferation of pulmonary arterial smooth muscle cells, thereby playing an important role in structural remodeling of the pulmonary arteries and in the development of hypoxic pulmonary hypertension.

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The changes in small pulmonary arteries of 15 patients with chronic obstructive pulmonary disease (COPD) were investigated by light and electron microscopy, image analysis etc. It was found that the structural changes in the pulmonary arteries of the patients with COPD were characterized by muscularization of non-muscular arterioles, media hypertrophy, longitudinal smooth muscle bundles in the intima and fibrosis in both the media and intima. In the course of time, these lesions resulted in thickening of the arterial wall and narrowing of the lumen. Clinically, the patients developed pulmonary hypertension causing cor pulmonale. Initial data on the structure of arterial wall at different segments were compared statistically. There was very significant difference between the COPD and control groups (P less than 0.001). By Fisher's auto-classification (automatic pattern recognition), the rate recognized was correct in more than 90% in the small arteries of less than 200 microns in diameter. It is suggested that these arteriolar changes are closely related to pulmonary hypertension. The image analysis showed that the ratios of MWA/MVA and MWT/MD were of great value in evaluating the degree of the changes in the arteries of the patients with COPD.

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The preventive effect of Radix Salciae Miltiorrhizae (RSM) on pulmonary hypertension (PHT) and right ventricular hypertrophy (RVH) induced by monocrotaline (MCT) in rats was observed with the methods of measuring the right ventricular systolic pressure (PVSP), the ratio of the right ventricle to the left ventricle plus interventricular septum RV/(LV+S) and the pulmonary small artery morphological analysis. The results show that RSM can reduce the PHT, and prevent the RVH and the increase of the medial thickness of pulmonary small arteries. It can also prevent the endothelial cell injury produced by MCT. The pharmacological effects of RSM on pulmonary circulation were also discussed.

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The monocrotaline-induced structural changes of small pulmonary arteries in rat and their relationship with pulmonary hypertension and right ventricular hypertrophy were observed by determining the right ventricular systolic pressure, and by light and electron microscope and morphometry. One to 38 days after last injection of monocrotaline (MCT), a medial thickening and lumen marrowing of the circular muscular arteries (CMA), accompanying terminal (TB) and respiratory bronchioles (RB), were found. And there after the lumen of CMA, accompanying TB, became dilated, and its medial thickness (MT) decreased, whereas the histopathologic changes of the partially muscular arteries (FMA), accompanying RB, became severe, their MT increased continuously, and finally reached the peak value on Day 50. At the first day after last MCT treatment, inflammation and muscularization were found in PMA and nonmuscular arteries (NMA), and became more severe with the cause of disease. Therefore, the intra-acinar pulmonary arteries, both CMA and PMA, increased in number while the NMA decreased in number significantly because of the structural remodeling. Four days after MCT treatment, the right ventricular systolic pressure began to rise, and reached its peak value on Day 50. Eight days after MCT injection, right ventricular hypertrophy developed, and became most significant from Day 23 to Day 30. The results suggest that structural remodeling, i.e. muscularization, of intra-acinar pulmonary arteries plays an important role in the development of pulmonary hypertension and right ventricular hypertrophy.

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Rabbits and rats were infected intratracheally with extracellular enzyme of Streptomyces thermohygroscopicus (H9-4) by only one exposure, and lesions of the lung developed including mononuclear macrophage infiltration as well as bronchitis and vasculitis. The obvious damages in type I pneumocytes, endothelial cells of capillaries and arterioles in the lung were observed by electron microscopy. Immunofluorescent histochemistry examination revealed exudation of plasma fibronectin which might play an important role during the process of lesion repairing in lung. The experiment also confirmed that extracellular enzyme of Streptomyces thermohygroscopicus might directly damage the lung tissue. These experimental data may serve as valuable reference for studying the etiology and pathogenesis of farmer's lung disease.

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There were 48 strains of thermophilic actinomyces isolated from the specimens of mouldy hay and sputum of the patients suffering from farmer's lung (FL). Streptomyces thermohygroscopicus (STHs), one strain of them, was used for this investigation. The microorganisms were injected into the lungs of rabbits and rats by thyrocrico- or tracheocentesis. The results showed that the pathological changes in the lungs including macrophage alveolitis, granuloma formation and diffuse interstitial were similar to that induced by other thermophilic actinomyces. IgG and C3 deposition in the lesions were also observed by immunofluorescence examination. Specific immunocomplexes in the sera of some animals were detected by ELISA with the STH-antisera. The results suggested that STHs was possibly one of the pathogens responsible for FL in China's countryside.

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Rabbits and rats were infected intratracheally with extracellular enzyme of streptomyces thermohygroscopicus (H9-4) for only one exposure and lesions of lung developed which included mononuclear macrophage infiltration as well as bronchitis and vasculitis. The obvious damages in type I pneumocytes, endothelial cells of capillaries and arterioles in the lung were observed by electron microscopy. Immunofluorecent histochemistry examination revealed exudation of plasma fibronectin which might be important to play certein role during the process of wound repairing in lung. The experiment also confirmed that extracellular enzyme of streptomyces thermohygroscopicus might directly damage the lung tissue, and these experimental data may serve valuable reference for studying the etiology and pathogenesis of farmer's lung diseases.

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