Chronic hypoxia results in pulmonary hypertension due to vasoconstriction and structural remodelling of peripheral lung blood vessels. We hypothesize that vascular remodelling is initiated in the walls of prealveolar pulmonary arteries by collagenolytic metalloproteinases (MMP) released from activated mast cells. Distribution of mast cells and their expression of interstitial collagenase, MMP-13, in lung conduit, small muscular, and prealveolar arteries was determined quantitatively in rats exposed for 4 and 20 days to hypoxia as well as after 7-day recovery from 20-day hypoxia (10% O2). Mast cells were identified using Toluidine Blue staining, and MMP-13 expression was detected using monoclonal antibody. After 4, but not after 20 days of hypoxia, a significant increase in the number of mast cells and their MMP-13 expression was found within walls of prealveolar arteries. In rats exposed for 20 days, MMP-13 positive mast cells accumulated within the walls of conduit arteries and subpleurally. In recovered rats, MMP-13 positive mast cells gathered at the prealveolar arterial level as well as in the walls of small muscular arteries; these mast cells stayed also in the conduit part of the pulmonary vasculature. These data support the hypothesis that perivascular pulmonary mast cells contribute to the vascular remodelling in hypoxic pulmonary hypertension in rats by releasing interstitial collagenase.

The ultrastructure of the bronchial epithelium of three asthmatic girls was studied from material obtained during bronchoscopy. In all patients the large bronchi were lined with an altered pseudostratified ciliated epithelium having a severely damaged ciliary border. Injury to the ciliated cells was manifested by apical bleb formation, destruction of free kinocilia, pathological ciliogenesis, dilation of the spaces of the endoplasmic reticulum and Golgi complex, an increase in the number of vacuoles and lysosomes, and the appearance of altered mitochondria. The most outstanding feature of the epithelium was the marked hyperplasia of the goblet cells with the development of intraepithelial mucous glands. The mucous elements of the epithelium had discharged their mucus. Further, there were signs of mucus cell injury and degeneration. Squamous metaplasia of the pseudostratified epithelium was not observed.

Serious damage to the tracheal epithelium due to bronchoalveolar lavage (BAL) was recorded. Immediately after BAL 99 ± 2% of goblet cells were exhausted and degenerated. Their regeneration began 24 h after BAL resulting in hyperplasia of goblet cells with the formation of endoepithelial mucous glands. The most pronounced injury to the ciliated cells was apparent 2 h after BAL. BAL markedly impaired the ciliary border. The mean number of cilia/µm² fell to 1.5 ± 0.3/µm², then gradually rose to 7.5 ± 0.5/µm² (controls 9.7 ± 0.5/µm²). The morphological signs of impairment of the self-cleaning ability of the epithelium were the most pronounced after 24 h and were still present at the end of the experiment

The reaction of goblet cells in the rabbit tracheal epithelium caused by the intravenous administration of 0.1 mg and 0.5 mg of acetylcholine, respectively, was studied. Due to the cholinergic stimulation the goblet cells were overstimulated, the mechanism of their secretion was accelerated and after rapid evacuation of their secretion the secretory elements mostly degenerated. Due to the administration of both doses of acetylcholine more than 90% of goblet cells were stimulated to discharge their mucus. After administration of 0.1 mg of acetylcholine the reaction was more prolongated, but the peak values of the degenerated goblet cells did not differ significantly after administration of both doses of acetylcholine. Twenty min after administration of 0.5 mg of acetylcholine the signs of massive differentiation of new secretory elements were encountered.