The effects of carbonic anhydrase inhibition on CO₂ elimination in the lung were studied in terms of P_CO2, P_O2, PH, HCO₃^- and minute volume. The mongrel dogs were divided into four groups as shown in Table 1.
The following results were obtained.
A group: minute volume increased remarkably.
PaCO₂ and arterial blood PH lowered.
B group: minute volume increased moderately.
PaCO₂ raised, arterial blood PH and a-AD_CO2 increased.
C group: minute volume was held constant (Hyperventilation).
PaCO₂ raised and arterial blood PH lowered.
D group: minute volume was held constant (Hyperventilation).
PaCO₂ raised remarkably and arterial blood PH lowered.
The suppression of CO₂ elimination due to the administration of 50mg/kg of acetazolamide was clearly observed when bilateral renal blood vessels were ligated. This effects were more markedly seen when ventilation was artificially controlled. However, in intact dogs, the suppression of CO₂ elimination was not observed.
The lowered CO₂ elimination is presumed to be caused by inhibition of carbonic anhydrase present in the erythrocyte with acetazolamide administration.

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Fifty hospitalized patients with spontaneous pneumothorax have been reviewed during the past five years and six months. In view of the increasing incidence of this disease, we have realized its gradually growing importance to the examination and treatment of chest disease.
According to our data, spontaneous rupture of pleural blebs or bullae constitutes the most important cause of spontaneous pneumothorax.
As etiologic factors of spontaneous pneumothorax, active inflammation of a lung, particularly pulmonary tuberculosis, is not emphasized.
In terms of its incidence as broken down by age, patients in their twenties top the list with 28%, followed by those in their fifties, thus showing that its incidence assumes a sort of “two-peaks” pattern.
The causes of spontaneous pneumothorax among younger patients somewhat differ from those among older patients.
There is every reason to believe that the incidence of spontaneous pneumothorax among younger patients results, among other things, from the rupture of bullae or bleb due to constitutional factors without significant intratracheal pressure, and that the incidence among older patients involves also the rupture of emphysematous changes (bullae or blebs) of the lung induced by many other causes, such as coughing.
We have been led to believe the constitutional factors to be the cause of this disease, since the majority of these patients are twenty-five years old or younger, tall and slender, no other recognizable pulmonary diseases are found and the 11-OHCS levels in their blood are low. Moreover, this disease runs in the family, and we have experienced at least one case of spontaneous pneumothorax associated with Marfan's Syndrom.
In view of the fact that the method of treatment just using needle aspiration of pleural cavity results in a high rate of recurrence, we have made it our principle to use the method of catheter drainage and continuous suction (of the pleural cavity), in which no case of recurrence has been found.
However, thoracotomy and resection of blebs or bullae must be performed in the below-mentioned cases.
1. When no signs of pulmonary re-expansion are shown three days after drainage and continuous suction has been applied.
2. Younger patients with blebs and bullae observed through X-ray.
3. Patients with recurrent pneumothorax or chronic pneumothorax.
It must be noted at this point that since a patient who has his contralateral pulmonary function sharply reduced, e. g., a serious emphysematous case or contralateral pneumothorax developed during the operation, convalesces unsatisfactorily, the treatment with drainage, continuous suction and pleurodesis is preferable, and any thoracotomy must be resorted to with great caution.

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To investigate the mechanical behavior of the lungs in asthma, dynamic compliance and viscous resistance (esophageal balloon method), airway resistance and FRC (body plethysmographic method), and FEV 1.0 were measured following the inhalation of chemical mediators or allergen extract in 26 experiments on 22 asthmatic patients, and also after the administration of bronchodilators in 19 of those in whom the induced attacks were definite. They were calculated as the ratio of compliance (Cl) and conductance (reciprocal of viscous resistance=G_L, reciprocal of airway resistance=G_AW) to thoracic gas volume (TGV) and their changes were indicated in the per cent of initial values (these in saline inhalation). The provocation of asthmatic attack was induced by inhalation of nebulized solution of acetylcholine, histamine or allergen extract, with or without prior injection of atropine or propranolol, with increasing concentration of the solution until a definite change in transpulmonary pressure and FEV 1.0 was resulted.
Changes in the ratio of Cl, G_L and G_AW to TGV were simultaneous and of the same magnitude in the response to these mediators and allergen and did not demonstrate any definite difference in the mechanism of airway constrictions with these solutions. Prior treatment with atropine (3 cases) did not prevent the usual changes whilst intravenous injection of propranolol or two subjects induced attack in a patient and lowered the sensitivity to acetylcholine in the other.
Values after inhalation of 0.5% isoproterenol aerosol (7 cases), a isoquinoline derivative (0.5% AQ 110) (7 cases) or injection of epinephrine (1 case) were usually greater than those in the control state but the difference in the pattern of the response of the ratio to these bronchial spasmolytics was not apparent. Aminophylline differed from the above bronchodilators in that the intravenous injection (4 cases) induced immediate and pronounced increase in Cl but slow and mild one in G_AW. This suggest the difference of the affecting site (e. g., conducting or peripheral airways) in these drugs.
Measurement of FEV 1.0 was proved to be very useful for the evaluation of the reaction in provocation test and reliable to follow the response to bronchodilators.

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The effects of exercise on the blood gas and ventilatory mechanics were studied in patients with brochial asthma in remission.
The initial study, involving 7 asthmatic children, used moderate exercise on a bicycle ergometer for 5 minutes. Expired gas and arterial blood were collected simultaneousely before and during the last 2 minutes of the exercise. At rest there were marked hypoxemia and high (A-a) O₂ difference. The latter was slightly larger than the high (a-A) N₂ difference observd, indicating that the decrease in arterial P_O2 was mainly due to the lesions of the lung which were underventilated and overperfused. There was no apparent correlation between the magnitude of airway obstruction, as measured by the FEV_0.75 and MMF, and the (a-A)N₂ difference on 6 cases examined. During exercise it was shown that arterial P_O2 increased with a concomittant decrease in (A-a) O₂ as well as a drop in (a-A) N₂. In two cases blood pH and base excess decreased slightly indicating development of mild metabolic acidosis during exercise. Their blood lactate concentration and L/P ratio increased slightly.
The response was further studied in an additional 2 children and 8 adults with asthma using a controlled step exercise for 4.5 to 6 minutes. Pre- and postexercise measurements were made with bodyplethysmography and spirometry. A consistent, marked, transient increase in airway resistance immediately after exercise with gradual return to pre-examined levels was seen in 9 cases. The average of the maximum decrease in airway conductance /thoracic gas volume was 54.9% of the control values. In 2 cases the airway obstruction following exercise lasted more than 30 minutes. There was a rough correlation between the severity of the disease and the magnitude of the bronchial response to exercise but none between the response to sulfur dioxide and to exercise.
The possible contributing factors to the observed increase in arterial P_O2 during exercise and the decrease in airway conductance following exercise are discussed.

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At gas chromatographic analysis of gases in pulmonary physiology, either the peak height or peak area is measured for quantitative analysis. Peak height is easier and more accurate to measure than the peak area. Peak area on the record should depend on the amount of the gas introduced and calibration curve for peak area should be linear, however that for peak height is usually not linear.
In this work, effect of sample volume to linearity of calibration curve was studied to reveal that calibration curve showed good linearity using sample volumes of 0.05ml for analysis of O₂, N₂, and Ne, 10ml for CO and 1.05ml for CO₂. Reproducibility of peak height and range of error in quantitative analysis of these gases when these amounts of volume are introduced, were sufficient for practical use.

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To study the inter-relationships between the bronchial muscular activity and bronchial vasomotor tone, the changes in airway and in bronchial arterial system to the administration of isoproterenol, isoxsuprine, aminophylline and angiotensin into bronchial artery, and to the injection of serotonin and histamine into the pulmonary artery were tested simultaneously in the anesthetized and thoracotomized dogs.
The administration of isoproterenol, isoxsuprine and aminophylline into bronchial artery resulted in the dilatation of airway and of bronchial vasculature, while the administration of angiotensin resulted in the constriction of both systems. Since the results were different from the previous findings, where the reverse relationship were observed in the changes of both systems following the injection of serotonin, histamine, acetylcholine and 1-epinephrine into bronchial artery, the different mechanism might be suspected that these agents acted directly on the smooth muscle of airway and of bronchial artery.
The administration of serotonin and histamine into pulmonary artery in the preparation where the bronchial artery was separated from the systemic circulation, also produced the dilatation of bronchial vasculature. No marked changes were observed following the section of vagi and thoracic sympathetic nerves.
From these results it was concluded that there is an intrinsic mechanism between airway and bronchial artery such as increased bronchial muscular activity may result in a secondary bronchial vasodilatation.

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We reported cases of bronchial ramification abnormalities, incidence, abnormal ramification type and some comments on relation to its abnormality and bronchiectasia in Japan.
Although almost all these cases are revealed by chance under a diagnosis of pulmonary tuberculosis and bronchiectasia of its part is seemed to result from pulmonary tuberculosis, we observed from the point of bronchiectasia and its disposition. Until now these abnormalities have been reported from surgeon, but chest physician must call attention to above mentioned points.

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A case was a 58 year old female with chief complaint of bloody sputa. She had a fit of facial frushing several times during eight months.
The chest X-ray revealed an atelectasis with tumorous shadow in the right upper lung field.
A tumor was found in the right main bronchus by bronchoscopy, and right pneumonectomy was performed.
Histologically the tumor was carcinoid. Electronmicroscopically the tumor contained many characteristic serotonin granules of the so-called neurosecretory type, round, electronopaque, with an average diameter about 2000Å, limited by unit membrane in the cytoplasm of light cells or dark cells.
Significant high level of serotonin 666mcg/1 was found in serum, and 5HIAA 33.3mg/24hrs in urine.
After operation, attacks of cramp-like abdominal pain occured frequently, so laparoscope was performed, and was detected metastasis in both lobes of the liver.

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Pulmonary alveolar microlithiasis (PAM) is a rare disease, but in Japan about 60 cases have been reported hitherto, including only one autopsied case. We had the second as an autopsied case.
A 55-year-old male was on March 30, 1967, first admitted to our clinic because of cough and dyspnea which followed a cold. All of his family had good health including his grandparents and his children and there appeared to be no known pulmonary problems in the family. In 1954 he was pointed out the pathologic findings in the chest x-ray accidentally, but no certain diagnosis was made and he had no respiratory symptoms. We could obtain those roentgenograms showing very finely mottled diffuseness of the lesion with greater density toward the bases and the cardiac outlines and diaphragms were indistinct due to the process. These roentgenographic and his clinical course were very suggestive of the PAM.
The roentgenograms of his chest on admission showed far advanced stage of the disease, i.e. in addition to the numerously increased mottled processes there were many thickened linear shadows and those of thickened pleura and emphysematous blebs. In laboratory data decreased vital capacity and P_O2 were conspicuous. After leaving hospital on June 3, he was re-admitted for severe dyspnea, it worsened helplessly and he died on October 24, 1967.
On autopsy, the lesion was revealed to be PAM and in lungs adding to the microlith-formation, there were diffuse fibrosis, subpleural emphysematous blebs and the thickening of the pleura and other organs (liver, spleen, kidneys) showed chronic congestion assosiated with chronic cor pulmonale.
Histologically, except for the intraalveolar microliths, ossification and remarkable elastosis in the interalveolar septa were revealed in the lungs.
Chemical analysis of the microliths obtained showed that the predominant elements are calcium and phosphorus (85%) with traces of alminium and iron.
This case belongs to those which have revealed to be of very long course and to progress very slowly without any specific symptoms.

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