Cortisone and ACTH were given to rabbits used in Masugi-nephritis' anaphylaxis (Oue), from the stage of sensitization to that of anaphylaxis. The results were as follows : 1) In cases previously given cortisone, no decrease of γ-globulin was seen after anaphylaxis.2) In cases previously given ACTH, a decrease of γ-globulin did not show a fixed tendency.3) In control cases of Masugi-nephritis' anaphylaxis none given previously, γ-globulin decreased remarkably.4) Kidneys in cases given Cortisone showed no histological change compared with the normal ones.5) Kidneys in control cases of Masugi-nephritis' anaphylaxis showed typical glomerulitis.6) Glomeruli in cases of Masugi-nephritis' anaphylaxis treated with ACTH showed non-typical change.

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In spite of the numerous experimental studies on the excitability of the auricular muscle since Adrian's experiments in 1920, its relation to the mechanism for the genesis of auricular fibrillation has not been investigated in detail. The author studied the excitability of auricular muscles in dogs with particular emphasis to the change in excitability in anoxia and its relation to the genesis of auricular fibrillation. This study also included some observations on the atrio-ventricular conduction system and its reactions to anoxia.The dog was anesthetized with 10 per cent Oltopan Sodium I. V. and under artificial respiration the chest was opened and the heart was exposed. A bipolar electrode, each terminal of which was made of 100 micron insulated copper wire, was used. To provide each terminal with an arrow-head, approximately 1 mm. at the end of each wire was bent back at about a 30 degree angle and held in position with a drop of solder placed between the bent part and the main wire. The bipolar electrode, each terminal of which was protected by threading it through a 25 gauge injection needle, was thrust through the auricular wall and after the needle was withdrawn, the arrow-heads held the terminals securely at the endocardial surface. An electronic stimulator and a synchronizer were used in combination in order to deliver square wave pulses as stimuli in such a way that the interval between normal and extrasystolic beat as well as voltage and pulse duration could be varied at will. For recording, a three channel oscillograph and a dual beam cathode ray oscilloscope were employed to make a simultaneous recording of the auricular wave and stimulating wave. The experiments were done under normal sinus rhythm except a few cases where electric heart driving was substituted. Results in both instances were essentially the same. Anoxia was obtained by forcing the animal to breathe through an artificial respirator for 10 minutes, a mixture of 10 vol. per cent oxygen and nitrogen or 5 vol. per cent oxygen and nitrogen. Arterial O₂ saturation was determined by the Van Slyke's manometer to check the presence of anoxemia.The excitability of the auricular muscle was dependent upon the phase of the cardiac cycle (interval from the preceding contraction), and the strength and duration of the square wave stimulus.The length of the absolute refractory period was from 125 to 140 milliseconds, and that of the relative refractory period from 70 to 80 milliseconds, the total refractory period being approximately 10 milliseconds shorter than that of the ventricular muscle.In most cases the threshold of the left auricular muscle was lower than that of the right. The supernormal phase and the dip phenomenon were observed in three cases respectively; however no interrelationship was found between them. It was found that various conditions affected the presence or absence of the supernormal phase.Latent period, i. e., the interval between the delivery of the stimulus and the occurrence of the extrasystolic beat was longer, when the stimulus was given in the initial phase of the cardiac cycle; but it was shortest, when given in or around the dip. In many cases anoxia tended to shorten the latent period. The interval between the preceding auricular wave and the onset of extrasytoric beat, i. e., the coupling time was almost constant, when the stimulus was applied in the initial two thirds of the relative refractory period.In anoxic state, the threshold value of strength of the stimulus increased with an increase in the degree of anoxia. Mild anoxia only slightly affected the refractory period, while severe anoxia prolonged both the absolute and relative refractory period. The conduction velocity within the atria was scarcely affected by mild anoxia but was considerably delayed by severe anoxia.

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The mechanics of breathing were studied before and during acute hypoxia induced by a low oxygen inhalation in nine normal subjects, five males and four females. Three subjects inhaled 14.5% oxygen and six subjects inhaled 10% oxygen.During the hypoxia both functional and static compliance were decreased. However, the decrease of the functional compliance was greater than the decrease of the static compliance. Therefore, differences between the functional and static compliance increased during the low oxygen inhalation.There was a slight increase in inspiratory and expiratory mechanical resistance, especially in the expiratory resistance during the hypoxia.There was some correlation between the percent of reduction of the pulmonary compliance and the increase of the mean pulmonary artery pressures and to the decrease of the arterial oxygen saturation, but no correlation was found between the increased mechanical resistance and the arterial oxygen saturation.On the basis of these results, it seems likely that the decrease of the pulmonary compliance during the acute induced hypoxia will be caused by the increased tone of the pulmonary artery system attributable to increased pulmonary artery pressures. On the other hand the increase of mechanical resistance seems to be caused by the bronchoconstriction. Other causal factors of these changes were discussed.

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INTRODUCTION Professor Maekawa presented a theory that the ultimate cause of hypertension is the disturbance in ATP-ATPase system, particularly the discharge in the blood stream of the renal ATPase which has property of being activated by sodium and inhibited by potassium. With regard to the genesis of the arterial and arteriolar necrosis which often associates the malignant hypertension in man and experimental animal, opinions have been discrepant, some regarding such necrosis as the result of the elevated pressure, some ascribing it to two factors, elevated blood pressure and excretory renal failure, but some, on the contrary, insisting that elevated arterial pressure is not the indispensable cause of such necrosis. In order to expand the above theory of Professor Maekawa, the author tried to disclose the relation between hypertension and histological changes, employing dogs and rats which were made hypertensive experimentally. This paper aims to report on the author's histopathological study with various genetic types of hypertension.EXPERIMENTAL NEUROGENIC HYPERTENSION Nine dogs were operated upon for bilateral section of the pressoreceptor nerves and their blood pressure was messured 2 to 3 times a week thereafter. The method of the blood pressure measurement was that of direct puncture in the femoral artery. Animals were sacrificed after various (3∼190 days) periods of observation by means of venesection, and organs were taken out and immersed in 10% formalin solution, for fixation. Specimens were made zelloidine or paraffine-sections and stained with hematoxylin-eosin, and Van Gieson's or Masson's method.RESULTS 1) Following the section of the pressoreceptor nerves, there was an immediate elevation of the blood pressure. At this time kidney showed swelling and exudation in glomeruli.2) As time elapses after the section of the nerves, fluctuation in blood pressure became less and less outstanding, while arteriolar change in the kidney became more pronounced. However, the degree of such change was independent of the degree of hypertension.3) Therefore, such vascular lesion as caused by this method evidently cannot be ascribed to the existing hypertension alone.4) Heart weight showed increase, but not proportionately to the degree of hypertension.

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Many investigators have observed that the coronary blood flow was markedly increased following the stimulation of the stellate ganglia and/or their cardiac branches. But as in previous report of our clinic pointed out, it cannot be concluded that the sympathetic nerve dilate the coronary vessels directly. From recent work of our clinic, it seems to be that the sympathetic nerve constricts the coronary vessels, and that the augmentation of coronary blood flow following the sympathetic stimulation chiefly results from the hemodynamic and metabolic changes induced. On the other hand, many workers suspected that the metabolites of the heart muscle released following the stimulation of the sympathetic nerve dilated the coronary vessels. It is the purpose of present study to find out some vasodilatative substance in coronary venous blood, to clarify the nature of the sympathetic coronary vasodilatative effect.The outline of experimental method was almost the same as previous report. The left coronary artery of dog was perfused from the animal's own femoral artery. Then the peripheral ends of the cut stellate ganglia or vagal nerve were stimulated electrically and the coronary venous blood samples were obtained before, during and after the stimulation of the nerves. The blood samples were obtained six times in one experiment : before stimulation, during stimulation and 15 seconds, 1 minute, 2 minutes, 3 minutes after the stimulation. Then immediately one ml. of those blood samples were injected into the tubing leading to the coronary artery as in previous report performed.Results were as follows : 1. Coronary blood flow was markedly augmented after the injection of the coronary venous blood samples which were obtained during the stimulation of the sympathetic nerves or 15 seconds thereafter. On the other hand, the injection of the coronary venous blood samples obtained before stimulation or 1 minute or more thereafter did not augmented the coronary blood flow. In 6 among 11 cases such findings were observed. No significant changes of heart rate and blood pressure was observed after the intracoronary artery injection of coronary venous blood samples.2. The coronary blood samples obtained before, during, or after the stimulation of the vagal nerve did not affect coronary blood flow, heart rate and blood pressure.3. From this study, it is obvious that the coronary venous blood samples, which were obtained during the stimulation of the sympathetic nerve or 15 seconds thereafter, induced coronary vasodilatation. Since no remarkable hemodynamic changes were observed following the intracoronary artery injection of coronary venous blood samples, it is concluded that some vasodilatative substance present in those effective blood samples. It seems that this substance plays an important role in sympathetic coronary vasodilatation. The exact nature of this substance is not clear, but it is probably some metabolite, because the effective coronary venous blood samples were obtained during the time corresponding to the increase in vigor of cardiac contraction. The coronary flow patterns following the intracoronary artery injection of coronary venous blood samples were far different from those following the injection of epinephrine or norepinephrine, and therefore at least coronary vasodilatative substance thus demonstrated is not epinephrine or norepinephrine themselves.

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We have experienced two cases of primary pulmonary hypertension; a 9-year-old girl and a 20-year-old male. Both these cases had had several attacks of syncope. The girl had complained of dyspnea and slight cyanosis, especially on exertion. The pulmonary artery pressures were systolic 111, ditolic 60, mean 84 mmHg. Autopsy of this case revealed a marked pulmonary arterio-and arteriolosclerosis with some thrombosis but no evidence of embolism. The male had dyspnea and marked cyanosis on exertion, the cyanosis was investigated. The pulmonary artery pressures were systolic 89, diastolic 55, mean 68 mmHg and the pulmonary arterial wedge pressure was 11 mmHg. The pulmonary vascular resistance was very high.On 100% oxygen inhalation the arterial blood oxygen saturation went up to 100%. However, the saturation dropped to the level of 80% during exercise test even though 100% oxygen was administered. On the other hand the cardiac catheterization showed no left to right shunt at any level.Autopsy of this male revealed a patent foramen ovale, which permitted only one way shunting of right to left, and no other congenital or acquired cardiovascular abnormalities. A marked pulmonary arterio- and arteriolosclerosis without any evidence of pulmonary arterial embolism or thrombosis was revealed. These two cases can be regarded as so-called primary pulmonary hypertension.We found, however, on observation of the pulmonary vascular casts of the male a great number of arterial anastomosis between the bronchial and pulmonary arteries. We discussed the relationship between these arterial anastomosis and the primary pulmonary hypertension, and concluded that these arterial anastomosis can be considered as the sequelae of the fetal state and will have a causal effects on the development of plumonary hypertension by continuous shunting of left to right.

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