Fifty mongrel dogs were anesthetized with sodium pentobarbital and left thoracotomy was carried out under artificial ventilation. Acute pulmonary embolism was produced by air injection (1-2ml/kg B. W.) into the main pulmonary artery. Hemodynamics such as aortic and coronary blood flow measured by electromagnetic flow meter and efferent renal sympathetic or inferior cardiac sympathetic nerve discharges were recorded simultaneously. Afferent impulses from lung and aortic baroreceptors were recorded in the right cervical vagus. Hemodynamics and neural responses to pulmonary embolism were compared with and without vagotomy at the cervical levels. Arterial pO₂, pCO₂ and pH were measured by I. L. meter following pulmonary embolism.
Systemic mean blood pressure (S. B. P) fell to 70.3±19.2% (Mean±S. D.) without vagotomy and decreased to 77.4±20.4% in average with vagotomy compared to each control level, but both returned to pre-embolism level within 1-2 minutes. No significant difference between the with and without vagotomy groups appeared in the fall in S. B. P. Immediately after embolism, pulmonary arterial pressure (P. A. P) rose to 238±111% in average in the group with vagotomy and to 215±70% in the group without vagotomy then gradually returned to each control level within 10-20 minutes after embolism. Definite correlations were observed between the fall of S. B. P. and the rise of P. A. P. following pulmonary embolism, in both groups (both p<0.01). The aortic blood flow decreased and the coronary blood flow increased following pulmonary embolism. Heart rate remained unchanged in the group with vagi intact following pulmonary embolism, but significantly increased after vagotomy (0.02<p<0.05). Both discharges of efferent renal nerve and inferior cardiac sympathetic nerve decreased immediately after embolism, despite the fall in S. B. P., followed by marked increase of efferent spmpathetic nerve activities. The transient decrease in sympathetic discharges disappeared by vagotomy, and only the increase of sympathetic nerve response was observed immediately after embolism. Therefore, it is postulated that a pulmonary depressor reflex is responsible for the transient decrease in sympathetic nerve discharge and this transient decrease in sympathetic nerve activities may relate to the fall of S. B. P, following pulmonary embolism. The increase in afferent impulses from the lung in the right vagus nerve was associated with the rise of P. A. P. and a decrease in aortic baroreceptors activities was always associated with systemic hypotension after embolism. Arterial pO₂ decreased, pCO₂ increased and pH decreased, however, these values returned to control levels within 30 minutes after embolism.
From these results, it is suggested that the effects of pulmonary depressor reflex on systemic circulation are slight, but the interruption of blood flow plays the major role in the transient hypotension due to pulmonary embolism in anesthetized dogs. The lowering of systemic blood pressure after embolism is thousht to be improved by increases in sympathetic nerve activities caused by baroreceptor reflex and changes of blood gas tension.

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Alveolar-arterial O₂ tension difference (AaDO₂) and arterial-alveolar N₂ tension difference (aADN₂) were studied prior to and after the series of treatment performed on the group of patients who were accompanied by consistently impaired alveolar gas exchange but who revealed their ventilatory capacity mostly within normal limits. AaDO₂ and aADN₂ obtained on these 175 patients were 25.7±0.8 (mean±1 S. E. E.) mmHg and 15.2±0.5mmHg, respectively.
AaDO₂ obtained on 64 randomly chosen subjects out of the referred group of patients prior to and after oral administration of d, 1-alpha-tocopheryl nicotinate were 25.3±1.2mmHg and 17.9±1.2mmHg and corresponding aADN₂ for the referred subjects were 15.1±0.7mmHg and 9.4±0.7mmHg.
AaDO₂ obtained on 27 cases prior to and after the series of oral prednisolone administration was 27.1±0.9mmHg and 19.2±2.3mmHg and corresponding aADN₂ was 16.6±1.2 mmHg and 12.2±1.3mmHg.
Based on these observations the author concluded his study indicating consistent improvement of impaired ventilation-perfusion ratio distribution in the lungs after oral administration of d, 1-alpha-tocopheryl nicotinate or of prednisolone seen on the patients with clinically-assumed “so-called bronchiolit is syndrome”. No statistically consistent difference on the effect of these two treatments was indicated.

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We have previously reported that the selective radiation of the rat trachea produced histological features similar to those seen in the lungs of the autopsy cases of congenital esophageal atresia associated with tracheoesophageal fistula. The present communication describes biochemical findings obtained in conjunction with histologic studies.
Twenty male rats of Donryu strain weighing 200-310g were subjected to lineac X-ray radiation exclusively of the trachea at a dose of 500 rads per day for 30 consecutive days. The rats were sacrificed 35 days after completion of radiation schedule and their lungs were removed for lavage to measure alveolar surfactant, cellular components and rate of surfactant synthesis after intravenous injection of C¹⁴ palmitate. The levels of pulmonary surfactant and cellular components in the alveolar space were much higher in the experimental rat than the control. The removal rate of surfactant from the alveolar space was sigficantly reduced in the experimental rat.
The results of these studies indicated that depletion of cilia associated with squamous metaplasia of the tracheal wall induced by selective X-ray radiation resulted in an accumulation of surfactant and macrophages in the alveolar space. These findings are consistent with the view that at least part of the pulmonary surfactant and alveolar macrophages is removed from the airspace via the respiratory tract by means of the mucociliary transport mechanism.

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Out of 500 patients with asthma at the allergy clinic of Tokyo Kyosai Hospital there were 5 patients with pulmonary infiltration with eosinophilia (PIE syndrome) in whom a specific diagnosis was established. The diagnosis was chronic eosinophilic pneumonia, allergic bronchopulmonary candidiasis, allergic granulomatous angitis (one case each), and chronic bronchitis (two cases). Common symptoms were asthma, fever, weight loss, leucocytosis, large volume of sputum and productive cough. Skin tests to common inhalant antigens were principally negative except for molds. Precipitins to Candida albicans were positive in the patient with allergic broncho-pulmonary candidiasis in whom late asthmatic reactions were provoked by inhalation of Candida albicans extract. Sputum cultures from the patients with chronic bronchitis repeatedly yielded heavy growth of pseudomonas aeruginosa. Serum IgE levels were generally low, ranging from 40 to 700ng/ml. The clinical manifestations, the skin test reactivity and the presence of precipitating antibodies to molds, pseudomonas etc. were suggestive of combined reaginic and Arthus type hypersensitivity in these cases. Their clinical features were similar to those of infectious type asthma. Therefore the possibility that Arthus type and/or cell-mediated sensitivity might be playing a part in some of the respiratory symptoms observed ininfectious asthma was suggested.

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慢性関節リウマチで加療中の51歳の家婦が, 膀胱炎を合併し, ニトロフラントイン内服10日目に, 全身倦怠感, 多関節痛, 発熱, 咳漱, 前胸部痛, 嘔吐をみとめた. 胸部右側背下部で小水泡性ラ音を聴取し, 胸部X線写真上両側下野に肺水腫様の陰影をみた. これらの諸症状は数日で改善したが, 再度の内服の2時間後に全く同じ症状が出現した. 末梢血好酸球増多と一過性のIgE値の上昇をみ, 即時型アレルギー反応の関与を示唆した.

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