To investigate the possible role of the biosynthesis of prostaglandins in the lung in the circulatory and airway dynamics, arachidonic acid, a precursor of prostaglandin E₂ and F_2α, was infused into the pulmonary artery in the guinea pig lungs. The following results were obtained.
1) Intravenous administration of arachidonic acid (A. A.) caused a dose-related decrease in systemic arterial pressure and increases in right ventricular and airway pressures in vivo.
2) These effects were specifically inhibited by indomethacin, but not influenced by either bilateral vagotomy, anti-serotonin, anti-histamine drugs or α-adrenergic blocade.
3) A. A. caused marked increases in perfusion and airway pressures also in isolated perfused lungs. Prostaglandin-like substances which contracted the stomach strip and rat colon were detected in the venous effluent immediately after A. A. infusion.
These results suggest that ciculatory and airway responses caused by A. A. are mediated via its conversion to prostaglandins. The opposite effects of A. A. infusion on systemic blood pressure and on airway and perfusion pressures may sugges the difference in the reactivity of tissues to prostaglandin E₂ and F_2α, and/or a preferential synthesis of these prostaglandins in the tissue. The cell involved in the rapid synthesis of prostaglandins in the lung might be the pulmonary capillary endothelial cell.

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The purpose of the study is to assess sequential effects of unilateral Bronchography on pulmonary function by using 4 different contrast media; namely, Urokolin, Dionosil (aqueous), Dionosil (oily) and Hytrast.
Forty-two patients with various chest diseases except for acute inflammatory lesions were subdivided into 4 groups and on each group unilateral bronchongraphy was performed using one of the contrast media. Perfusion lung imaging, flow-volume loops and chest radiography were obtained immediately before and, 4, 24, 48, 72 hours and one week after unilateral bronchography. ^99mTc-MAA was injected for perfusion lung imaging except at 4 hours after bronchography when ¹³¹I-MAA was used. Perfusion distribution was calculated by measuring radioactivity of each lung. Functional loss of ipsilateral perfusion following bronchography was calculated by Birath's formula proposed for bronchospirometry.
Ipsilateral perfusion decreased most markedly immediately after bronchography and gradually recovered in 24 to 48 hours. Influence on V₅₀ and V₂₅ (maximum expiratory flow rate at 50% and 25% of vital capacity, respectively) was the greatest, indicating that the small airways were affected most seriously. It was especially so if either Hytrast or Dionosil oily was used as a contrast medium. It took longer than 72 hours for recovery of V₅₀ and V₂₅ to the control level. All four contrast media were cleared from the major airways in 24 hours, forming acinar or millimeter patterns in the lung parenchyma. Hytrast appeared to remain in the lung for a longer period than the other 3 contrast media.
In summary, Hytrast seems to cause the most serious and prolonged derangement of pulmonary function, followed by Dionosil (oily). Dionosil (aqueous) and Urokolin had the least effect. It is speculated that the reason for an early recovery of perfusion, despite a prolonged effect on V₅₀ and V₂₅ is due to establishment of collateral ventilation distal to the small airways.

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The Clinical, and light and electron microscopic pictures of a patient (43 year-old male) with desquamative alveolitis were presented.
As diffuse pulmonary infiltrations were seen radiologically and slowly progressive pulmonary symptoms were observed, open lung biopsy was performed. The clinical and histologic findings were characteristic of desquamative alveolitis as described by Liebow et al. By electron microscopy the desquamated intra-alveolar cells comprised three groups. These were granular pneumocyte, its premature cell, and alveolar macrophage. The intra-alveolar cell population was found to consist of approximately 80% granular pneumocytes, including premature cells, and about 20% alveolar macrophages.

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A case of unilateral hyperlucent lung was reported. The main roentgenologic features of this disorder were hyperlucency of the affected lobe and decreased peripheral vascular markings with a small hilar shadow. A bronchogram of the affected side showed a slight dilatation and the irregular calibre of the basic bronchi. In contrast, the upper branches were thin and poorly filled. An angiography of the left upper lobe artery revealed that the blood vessels were very small.
The pulmonary function and the bronchospirometric studies of this patient revealed markedly reduced ventilation and perfusion of the affected lung. The cause was unknown, but the possible factors that might have caused this condition were reviewed.

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A case of macroglobulinemia, 68-year-old male, is presented. The chest X-ray film revealed infiltrative-reticular shadows and pleural thickening especially in right lower field. The diagnosis was established by both characteristic monoclonal increase of IgM(L) in the serum and remarkable infiltrate of plasmacytoid-lymph-reticular cells in biopsied lung, pleura and lymph node tissues.
Pleuropulmonary lesions were responsive to cyclophosphamide, but not to chlorabmucil. The patient died in coma 1 year and 8 months after the first visit.

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