Lipid peroxidation as an effect caused by the exposure of respiratory tissue to ozone has been suggested by several investigators. Vitamin E is believed to function as a “scavenger” of free radicals, thereby interfering with the propagation of the peroxidation reaction. The protective effect of vitamin E on ozone toxicity in rats was investigated at the ultrastructural level by scanning and transmission electron microscopy. Adult rats (130g) were placed randomly into two dietary groups. One group was fed a diet free of vitamin E, and the other, a diet containing 100mg of dl-α-tocopherol (vitamin E) acetate per kilogram of diet. After 98 days of dietary treatment, both groups were exposed to 0.29±0.08 ppm (mean±SD) ozone for 3 hours daily in an acrylic exposure chamber for 16 consecutive days. Animals from each group were killed immediately after ozone exposure, on the 5th, 11th and 16th days.
The lungs were removed, fixed at a distending pressure until the pleural surface became smooth and processed for electron microscopy. The following ultrastructural findings were more prominent in the vitamin E-depleted group than in the group whose diet contained the vitamin:
1. Numerous small round bodies were found scattered on the bronchial surface and cytoplasmic protrusions of non-ciliated bronchial epithelium were increased in number, suggesting increased bronchial secretions. Clara cells were accompanied with many small swellings and small round bodies on their surface.
2. Swelling or denudation of the cytoplasm of the Type I alveolar surface lining cells with exposure of the basement membrane (so-called alveolar ulcer), and focal swelling of the cytoplasm of the Type II alveolar cells. The extent of these changes was most marked after 5 days of exposure.
3. Considerable cell debris was found in the alveolar spaces, due possible to cellular damage.
4. After 16 days of exposure, both alveolar interstitium and basement membrane were edematous and were greatly thickened.
The morphological results tend to support the biochemical evidence that one effect of vitamin E is to prevent or alleviate the cytotoxic effects of ozone.

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1) The over-all association velocity constant (Kc) for the combination of oxygen with human red blood cell suspensions at 0% initial saturation have been measured in a consinuous flow rapid reaction apparatus with oxygen electrode.
2) Kc of 13 normal control measurement were in between 110 and 215 mM^-1 sec^-1, and mean ±S. D. was 144.5±25.9 mM^-1 sec^-1. These values were in good agreement with previously reported values. Repeated measurement of two identical cases showed approximately close value.
3) Because of relatively large variation of individual Kc value, caution should be paid to use it for calculation or simulation of pulmonary oxygen uptake process.
4) Kc after alteration of chemical constituents of the red blood cell membrane have been measured as a new approach to investigate whether red blood cell membrane is a barrier to oxygen diffusion.
5) Sulfhydryl residues were inhibited by irradiation and treatment with mercurials. The Kc of treated red blood cells were not different from control. This result suggests that the sulfhydryl inhibition has not a significant effect on the rate of the red blood cell O₂ uptake.

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The octapeptide, angiotensin II (AII), is made from the relatively inactive angiotensin I (AI) by the action of angiotensin converting enzyme (ACE) in the pulmonary circulation. AII is one of the strongest vasopressor agents and has been investigated for many years as a cause of essential hypertension.
The present investigation showed the effects of AII on the contraction of rabbit pulmonary artery and aorta with various vasoconstrictors.
Male rabbits weighing 2.7-3.0kg were killed, the pulmonary artery and the descending aorta were removed and suspended in a bioassay glass chamber superfused with Krebs-Hensleit solution at 37°C saturated with oxygen and carbon dioxide (95: 5, v/v).
Tissue contraction was detected by an isotonic transducer (ME Commercial, Tokyo, Japan) and recorded using a polyrecorder.
1) Rabbit aorta strip showed a bigger contraction than the rabbit pulmonary artery strip with the same dose of AII.
2) The effects of various vasoconstrictor agents on the rabbit pulmonary artery and the descending aorta strip were remarkably increased with continuous infusion of a low dose of AII (0.5ng/ml).
3) These results suggest that AII by itself acts on the vascular smooth muscle directly as a vasoconstrictor agent and that AII also acts on the vascular smooth muscle indirectly by potentiating the effects of various vasoconstrictor agents such as catecholaminesete. And these two mechanisms may play a role on the regulation of pulmonary and systemic arterial blood pressures.

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Asthma is a clinical syndrome manifested by reversible and intermittent obstruction of the bronchi. Over the past several years numerous in vivo studies have indicated that asthmatic individuals are deficient in their response to β-adrenergic agents, compounds that are known to raise cyclic AMP levels in many tissues. In such a case steroid therapy provides the marked relief, but the mechanism of this steroid therapy is still unknown.
Present investigation was done in an effort to clarify the mechanism of steroid therapy in an asthmatic patient. Male guinea-pigs, weighing 250-300g, were killed. Guinea-pig trachea (GPT) was removed and suspended in a glass chamber and superfused with Krebs-Hensleit solution at 37°C saturated with oxygen and carbon dioxide (95: 5, v/v). Contraction and relaxation of GPT were detected by an isotonic transducer and displayed on a polyrecorder.
1) GPT showed contractions with acetylcholine, histamine, serotonin, prostaglandin F_2α and bradykinin. And these contractions became smaller with continuous infusion of prednisolon (5μg/ml).
2) GPT showed relaxations with isoproterenol, neophyllin and prostaglandin E₂. And these relaxations with isoproterenol and neophyllin became bigger with continuous infusion of prednisolon (5μg/ml), but prostaglandin E₂ showed no increase of relaxation.
3) These results suggest that prednisolon increases the effect of pronchodilator and decreases the effect of bronchoconstrictors.

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53才, 男. ホジキン病にて VEMP 療法を行い, 良好な経過をとつていたところ, 熱, 咳・痰とともに胸部X線像で右下肺野に異常陰影が出現した. 次いで右胸膜炎を合併し, 胸水中より Nocardia. asteroides が検出され, 肺ノカルジア症の診断のもとにサルファ剤などの化学療法を行つたが, 気胸を併発, 呼吸不全にて死亡. 剖検にて病巣中に同菌の菌糸を証明した.

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23才女性. 咳嗽及び胸部異常陰影を主訴として来院. 胸部線検査では, 右上前縦隔に巨大な球状陰影を認めた. 諸検査にて, 奇形腫あるいは悪性胸腺腫を疑い手術施行, 病理学的検査にて, 胸腺ホジキン病と診断された1例を呈示する.

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