In sixteen hospitalized patients without cardiopulmonary disease (a control group), six patients with pulmonary diseases, five patients with myxedema and sixteen cardiac patients, the so-called sensitivity of the respiratory center to the carbon dioxide and hydrogen ion stimulus has been determined by relating effective alveolar ventilation to changes in arterial CO₂ tension and hydrogen ion conentration induced by CO₂ inhalation.1) In the control group (VA/m²)/(Pa_CO2) was within the range of 0.39 to 0.9 1./min./m²/mm. Hg and (VA/m²)/((H⁺)a) was within the range of 0.6 to 1.2 1./min./m²/10^-9 mole/1.2) Three patients with emphysema (group III, IV after Baldwin's classification) and one patient with myxedema revealed a reduced sensitivity as compared with the normal control group. In this reduction of sensitivity, in emphysema, acclimatization to the increase of arterial carbon dioxide pressure seemed to be the chief causal element and sometimes mechanical impairments of breathing might have play a part. In myxedema, hypofunction of the thyroid which is a link in the adrebal sympathetic system seemed to be an important factor.3) Cardiac patients, especially in the presence of congestive heart failure, revealed an increased sensitivity as compared with the control group. In such increase of sensitivity, acclimatization to the decrease of arterial carbon dioxide pressure seemed to be the important causal element. Metabolic acidosis and others were discussed.

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In the Part I. I have reported that there were observed the respiratory changes i.e. tachynea and labored respioration in rabbits, into which cervical subarachnoid space almina-cream were injected, but its pathogenesis has been difinitely unknown.Now in this study I examined the respiratory responses upon the electrical stimulation of spinal cord at the cervical (C. 3-4) or thoracic (D. 1-5), adding some spinal transection or vagal section. Electrical stimuli were given in the form of thyratron discharges (50 cps) or an alternating commercial current (60 cps). Their output voltage was between 1.5 V. and 10 V.Results obtained are as follows.1. Electrical stimulation at the cervical level resulted in the inspiratory, midpositional and expiratory apnea or tachypnea.2. Stimulation at the thoracic level resulted in either apnea or tachypnea, but in most cases the latter ones.3. By the additional stimulation at the thoracic level, the apneustic responses upon the stimulation at the cervical level relieved and respiratory movements reappeared.4. During the tachypnea or apnea evoked by stimuli at the cervical level (C. 3-4), electrical discharges of the external intercostal muscles increased. Such discharges suddenly initiated with the maximal intensity, continued during a long inspiratory phase and further remained for the short expiratory phase.5. When the electrical stimuli were applied in the dorsal areas of the spinal cord after section of both vagal section, the rate and the amplitude of the respiration extremely increased.6. After only one spinal segment was isolated by spinal transection, the stimulation of this segment at the ventral area resulted in apneustic responses but at the dorsal area resulted in no remarkable respiratory responses.

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On 13 patients with pulmonary tuberculosis, work load was placed by bicycle ergometer and their cardio-pulmonary functions were studied by means of cardiac catheterization.The results were as follows : In minimal and moderately advanced cases, an increase in pulmonary arterial pressure and cardiac index, and a decrease or unchangeability in total pulmonary vascular resistance were found. In far advanced cases or in cases with such complications as pleural effusion, emphysema and pleural callosity, O₂ removal showed a marked decrease and cardiac index decreased, neverthless, a marked increase in pulmonary arterial pressure and total pulmonary vascular resistance were found, and in advanced cases work load was limited within low range.

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It has been observed by many investigators, especially by Comroe & Schmidt in 1938, that (1) Carotic body is reflexible respiratory regulation centre acting as the chemoreceptor, and (2) Hypoxemia, acidosis and accmulation of PACO₂ in blood stimulated this centre. Also Lambertson & Shephard have reported on respiratory response in healthy man to the inhalation of oxygen at high atmospheric pressure.The author has examined the pulmonary function in patients of heart diseases, and also made a study of both respiratory response and circulatory dynamics under highly concentrated oxygen inhalation at 1 atmospheric pressure in both normal men and patients with heart diseases.20 patients who suffered from mitral diseases, aotric disease, myocard infarction and hypertensive heart diseases were divided into 2 groups : Group I, 12 with cardiac compensation ; Group II, 8 with cardiac decompensation.Pulmonary function was tested by Benedict-Roth's respirometer. Also, changes of Respiratory minute volume between normal cases and patients in 40-50% oxygen inhalation at 1 atmospheric pressure for 20 minutes were observed.Alveolar gases, and O₂ content, CO₂ content, PH, and PCO₂ of arterial blood were observed, before and after 5 minutes from the beginning of oxygen inhalation.CO₂ content and O₂ content of the blood samples collected from puncture of femoral artery were determined manometrically by the technique of Van' slyke and Neill, alveolar gases were done routinely by gasmetry (Roken-shiki) and arterial pH by electric pH-meter.Results obtained from these experiments are as follows : (1) Disturbance of the pulmonary function in patients in most clearly seen in proportion to the degree of decompensation. In decompensated group, the obtained results revealed prominent decrease, as follows : up to 48.7% of predicted value in Vital capacity, 17.7% of p. v. in Expiratory reserve volume, 43.0% of p. v. in Maximum breathing capacity, 68.9% in Ventiratory reserve ratio, and showed 0.88 in Air velocity index. However, Respiratory minute volume showed an increase of 43.3% due mainly to increased Respiratory rate ; and the Respiratory equivalence became 4.1. So, it is presumed that secondary pulmonary congestion in the decompensated group causes the disturbance of Ventiration.(2) As to Respiratory minute volume, it was observed that after 10% initial decrease the Respiratory minute volume was increased 16% (average), followed again by depressive tendency in normal men under oxygen inhalation at 1 atmospheric pressure, while in decompensated patients, marked depression continued in proportion to the degree of decompensation.(3) As to Alveolar gases, O₂ concentration in alveoli increased in all cases in both groups ; but in regard to the CO₂ decrease, patients of decompensation revealed a disturbance of ventiration, mainfesting the least decrease with a rate of 9.3% as compared with cases of normal men (decrease ratio of 19.9%) and compensated patients (decrease ratio of 12%).(4) As for Arterial pH, I observed alkalosis in normal men on the average of +0.032 and in compensated patients +0.022, while acidosis averaged -0.002 in decompensated patients.(5) About PACO₂ in blood, decompensated patients showed the elevated tension on the average of +2.86 mmHg compared with decrease in CO₂ tension which normal men (average -4.34 mmHg) and compensated patients (average -0.61 mmHg) manifested.In conclusion, healthy men who were administered highly concentrated oxygen at 1 atmospheric pressure showed alkalosis, and a decrease in PACO₂ and in CO₂ content in alveoli ; while on the other hand, decompensated patients under the same conditions showed acidosis, elevation of PACO₂, and the smallest precentage among the groups of decrease in alveolar CO₂.

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EXPERIMENTAL RENAL HYPERTENSION The author produced experimental renal hypertension in twenty adult dogs, 7.0-17.2 kg. weight, using the method of Goldblatt (12 dogs) and Page (8 dogs). Blood pressure was messured 2 to 3 times a week with the direct puncture in the femoral artery. In the course of this experiment, it was performed the clinical examination including the measurement of body weight, urinary volume and electrocardiogram. After the animals were sacrificed, the author examined organs histopathologically, with special reference to the relation of observed histological alternations to hypertension.The Results of this study were as follows : 1. Generally, the more pronounced the elevation of blood pressuer, the more marked the lesion in kidneys. However, in some of the cases, pronounced elevation occured in animals whose renal lesion was slight. To the contrary, in some cases elevation in blood pressure was minimal in the presence of moderately pronounced renal lesion. It seems that there exists no definite relation between the hypertension, it degree and duration, and the renal lesion.2. There was no lineary proportinal relation between the degree of renal lesion and the time allowed after the performance of the operation.3. There was no such relation that the hypertensive dog with excretory renal failure necessarily showed pronounced vascular lesion.4. Exudation in glomeruli, presumbly caused by abruptly developing pronounced hypertension, occured in small number of the case.5. There existed no relation of linear proportion between the degree of hypertrophy of the heart and the degree of hypertension or length of time allowed after the institution of the operation.6. Generally, the more pronounced the elevation in blood pressure, the more extensive the injuried area.

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The author, by means of ballistocardiogram, investigated the change of stroke volume and cardiac output in congestive heart failure, its recovering state and compensated state. They diminish with oliguria in congestive heart failure as many investigators said. But when patient recovers from it, they do not directly return to their normal value but they become too large with diuresis in recovering state and then diminish to normal value in compensated phase. These results suggest in one sense the supplementary or compensatory relation of heart and kidney i.e. one may say that when cardiac output diminishes, oliguria results that may increase venous return in order to enlarge stroke volume, and when cagrdiac output becomes too large in recovering phase, diuresis results that may diminish venous return in order to remove the load of heart. This too large stroke volume in recovering state may be one cause of too frequent embolia of brain in this phase.

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