Neurocircutatory asthenia (Oppenheimer) is thought to be functional circulatory or nervous disorder and anxiety neurosis, but its cause is still unknown. Prof. M. Maekawa concluded that almost of these neuroses may be conditioned somatically by subclinical arachnoiditis adhesiva cerebrospinalis.In this study, I observed the somatic responses and emotional behavior in rabbits, to which almina-cream were injected or vinyl tube filling up with almina-cream were inserted in spinal subarachnoid space. Results are as follows.1. Of 7 cases to which alumina-cream were applicated at the upper thoracic level (D. 1-5), there were sinus tachycardia in 6 cases, and the inverted T wave electrocardiographically in one case. In all 3 cases into which subarachnoid space the vinyl tube filling up with alumina-cream were inserted at the upper thoracic level (D. 2-7), there were, as electrocardiographic changes, the inverted T wave, the depressed ST segment and/or the supraventricular paroxysmal tachycaedia observed.2. Of 5 cases to which alumina-cream were applicated at the cervical level (C. 3-5), there were observed tachypnea in 3 cases and labored respiration in 2 cases.3. The histopathological findings of the hearts of 4 cases accompanied by the electrocardiographic changes showed thickening of the small or middle arteries, especially subendocardial, and accordingly degeneration or necrosis of the myocardial fibers, cell infiltration and proliferation of fibrous tissue around these arteries.4. The histopathological findings of the kidney of the thoracic group were degeneration of tubli and glomeruli, and interstitial cell infiltration.5. "Sham rage" (Bard) were observed in 4 cases of thoracic group and one case of cervical group.6. Alumina-cream were found histochemically in dorsal and central areas of spinal cord.

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After the sino-atrial border in a toad's heart was locally ligated, unipolar lead E.C.G. by means of simultaneous recording were made of the sinus venosus and different points on the surface of the atria, and calculated the activation times regarding points on the surface of the atria. At the same time the morphology of the P wave on the E.C.G. led from the surface of the atria was studied. Summary of the results is as follows : 1) When the border between the sinus venosus and the right atrium was ligated the activation times calculated for different points on the left atrium were found not to have been effected, but considerable delay at points on the right atrium was noted. This was supposed to be due to the fact that the stimulus proceeding from the sinus venosus was first conducted to the left atrium and then led into the right atrium over the border of the right and left atrial wall. Further, the fact that the activation time expended in the left atrium was found almost normal under such condition proved that the stimulus conduction to the left atrium must be carried out directly from the sinus venosus even in normal condition.2) When the bordering region of the sinus venosus and the left atrium was ligated no change was detected regarding the activation time at different points on the right atrium, but the activation time at those points on the left atrium was considerably delayed. It was then assumed that all these results lay in the fact that the impulse sent from the sinus venosus first enters the right atrium and then goes into the left atrium over the border of the right and left atrial wall.3) It takes about 0.04 second for an impulse to be conducted over the border of the right and left atrial wall. From this fact such a stimulus conduction may be looked upon as to undergo some resistance.Accordingly, it must be considerd that the activation of both atria in performed separately with the septum as marking the boundary of activation, and that the activation of both atria as a whole is not supposed to be of the nature of perfect diffusion.4) Ligation of the atrial septum does not affect the normality of the rhythm in the sinus venosus, or in the atrium, or in the ventricle, which proves that there exists no stimulus conduction pathway in the atrial septum directly convecting the sinus venosus and the atrium or the sinus venosus and the ventricle.5) The P wave registered on the unipolar lead E.C.G. taken over the surface of the atrium down below the ligated portion is found to show slurring and notching on its apex and sometimes such an unusual aspect as the splitting of the wave into two waves. So much is brought about here as a supplementary view to show what has been deemed some of the causes.In concluding above two reports it may be said that the impulse conduction in a toad's atria, though performed separately in the right and left atria, is not supposed to be wrought through the specific stimulus conduction pathway but to be of the nature of diffusion.

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There are three types of experimental hypertension : pressoreceptor denerved hypertension (Hering, 1927), renal hypertension (Goldblatt, 1934; Page, 1939), and DCA hypertension (Selye, 1943). In these hypertensions, much has been done for the research of cause of hypertension, but each of them can not explain the whole phenomenons of hypertension. Therefore, it is necessary to see the correlation to each other. Selye produced malignant hypertension as well as nephrosclerosis, acute nephritis, and albuminuria in animals by means of long-term administration of DCA. He attributed them to be due to an excess response of pituitary-adrenal system, which was called general adaptation syndrome. However, the relationship between hypertension and pituitary-adrenal system is not so clear that the influence of adrenal cortex on hypertension seemes to be questionable. The auther investigated the function of adrenal cortex by measuring 17-KS excretion in urine in hypertensive patients of various types, Goldblatt's and Page's renal hypertensive dogs, DCA-hypertensive rats, salt hypertensive rats, and also pressoreceptor denerved hypertensive dogs.Method of measurement of urinary 17-KS excretion The auther adopted Miyake's method where Drekter's extraction, Pearson's color reaction and Fraser's equation were applied on the basis of Zimmermann's color reaction.The 1st Experiment : The adrenocortical function in hypertensive patient.The auther performed measurement of 17-KS excretion in urine, of circulating eosinophils count, and 4-hour epinephrine test in hypertensive patients of various types, (one Cushing's syndrome, one acromegaly, 26 essential hypertension, 18 renal hypertension, and one pheochromocytoma) to see adrenocortical function.Results 1) 17-KS excretion in urine Essential hypertension : In 7 of 16 males it showed low values and in 9 normal values. In 6 of 10 females low values and in 4 normal.Renal hypertension : In 9 of 10 males it revealed low values and one normal value.Acromegaly : One male, normal value.Pheochromocytoma : One male, normal value.Cushing's syndrome : One female, high value. This was just one case which showed a high level of urinary 17-KS excretion.2) Circulating eosinophils count Essential hypertension : In 9 of 26 patients, it showed insufficiency.Renal hypertension : In 5 of 12 patients, it showed insufficiency.3) 4-hour epinephrine test Essential hypertension : In 11 of 14 patients, it showed insufficiency.Renal hypertension : In 5 of 6 patients, it showed insufficiency.Acromegaly : In one patient, it showed insufficiency.

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It is suggested that the disturbance of carbohydrate metabolism refers to the development of hypertension such as diabetics may be attended with hypertension. Phlorrhizin. 2. 4-dinitrophenol (DNP) and butyric acid were used to produce the patterns of the hypertension concerned in such metabolic disturbance.The results obtained were as follows : 1) Hypertension did not occur in the rats, in which glucose loading was given in a dosage just enough to produce glucosuria for the experimental production of the patterns of diabetic hypertension. When an increased dose of phlorrhizin was given every day in a quantity just enough to produce glucosuria, the blood pressure increased moderately in all rats to 140-150 mmHg. Loading with butyric acid or leucine led to further elevation of the blood pressure.2) The effects of DNP, which involves the disturbance of metabolism in whole body, on blood pressure were also observed. No remarkable change was produced on the blood pressure by DNP administration. The change in the kidney was slight. However, the necrotic fall of the peripheral body tissue was observed in rabbits and rats.3) It is said that butyric acid may be produced in the intermediary process of the fat metabolism. Accordingly, the pressor effect of this compound was studied. In long-term experiment, the blood pressure was moderately elevated in most cases. When some animals showed no elevation of blood pressure, they were subjected to a loading with leucine, and then the blood pressure rose slightly. The necrotic fall of the tail was observed in rats.4) Such pressor substances as phlorrhizin, butyric acid and leucine caused tachphylaxis in the animals.From the above results, it seems without a doubt clear that the disturbance of metabolism is responsible for hypertension. But such degree of slight and not strictly specific metabolic disturbance as was induced in the experimental animals in the present study by means of phlorrhizin and other chemical substances, was not striking enough in its effect to yield a satisfactory result, because the living oranisms were capable of adaptation. The truth is that these chemical substances constitute neither necessary nor sufficient condition for hypertension.

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In 53 patients with pulmonary tuberculosis, cardio-pulmonary functions were studied with aid of the right heart catheterization and subdivisions of the lung volume were measured.The results were as follows : With the progress of tuberculous lesion of lungs, pulmonary arterial pressure, volume of minute ventilation, cardiac index, pulmonary vascular resistance and work of the right heart against pressure increased, and then O₂ removal, arterial O₂ content and arterial O₂ saturation decreased. Pulmonary hypertension was attributable mainly to the increased pulmonary vascular resistance caused by the reduced pulmonary vascular bed. Cardiac index showed a positive correlation to O₂ uptake and negative correlation to arterial O₂ saturation and A-VO₂ difference. Generally, cardiopulmonary functions were relatively well compensated, and, in advanced cases, however, there was a possibility of appearance of chronic cor pulmonale.

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The author constructed a Ballistocardiograph, which consists of condensermicrophone, chair, balance and electric magnifying apparatus. When a patient sits on the chair, moving of human body by his circulation is received by the balance, and mechanical change of balance is converted to change of electric capacity by condensermicrophone which is magnified and recorded. The curve which is recorded by this apparatus, like that of Mr. I. Starr, consists of three main waves, e.g. I, J, K wave. Ballistocardiogram was compared with electrocardiogram and electrophonogram, and it was corroborated that I-wave was caused by the repercussion of human body when heart ejected the blood.

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I. Starr showed how to calculate stroke-volume from ballistocardiogram, where it was unconsciously presupposed that I and J wave could be treated as if they had one another no interference of hight. So the author then wanted to examine how much interference did I and J wave suffer one anoter. In order to investigate it, we must know the ideal I and J wave. And it presupposes the other question : what does ballistocardiogram show? Ballistocardiopraph, as the author uses balance, records the change of force caused by cardiac ejection and aortic impact. Starting from the conception of impulse, force is the first differential of momentum, and as specific gravity of blood may be practically regard as 1.0, we can assume that ballistocardiograms shows volume acceleration of blood circulation, especially of cardiac ejection and aortic impact. As to the question how to get volume acceleration of cardiac ejection not in vitro, we can get the help from law of Poiseuille, because first differential of law of Poiseuille showes the volume acceleration, and we see that volume accleration of cardiac ejection is a function of Tachogram of aortic pulse and width of any wave in ballistocardiogram is quite same as that of first differential of pulse. As width of main wave of tachogram is nearly 0.1 second, when tachograms is compared with that of ballistocardiogram, we can conclude that interference of I and J wave is almost negligible.

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As from previous report we see that ballistocardiogram is impulse wave in which I and J wave are caused respectively by cardiac recoil and aortic impact and height of I and J wave hardly interfere one another, we can easily calculate the momentum of cardiac ejection from ballistocardiogram.Formula for calculatioh is as follows : momentum of cardiac ejection =K₁(I+J)E or K₂(I+J)√(C) where K₁, K₂ : constant of apparatus E : ejection time C : cardiac cycle When this formula is established, we can deduce from it the formula for calculation of stroke volume as follows : K₁(I+J)E=Impulse =momentum (M×V) =Sv×Vm =Sv×Sv/A×E =Sv²/A×E so Sv=√(K₁AE²(I+J)) or K₃√(A(I+J)C) where Sv : stroke volume Vm : mean blood velocity in aorta

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The author reported the value of stroke-volume and momentum of cardiac ejection of normal subjects obtained by ballistocardiogram, and at the same time these methods of measurement were critically examined. As ballistocardiogram showes, as previously reported, the impulse wave of circulation which is mediated by human body, the values obtained by it inevitably contain some degree of inexactness. In quantitative investigation by ballistocardiogram if we want to get the minimum error of it, it is better to use the value of momentum of cardiac ejection, where survey of the relation of it to other physiologic functions is sacrificed. In order to supplement this weak point, one needs deducing stroke-volume from ballistocardiogram, though its value is not so exact. In the latter it is advisable to investigate the relative changes in same subject.

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The author investigated the influences of respiration, exercise, anemia on K wave of ballistocardiogram. At first in respiration, K wave augments in inspiration and diminishes in expiration. K wave augments also in exercise, in fever time, and in anemic conditions. In latter case it was observed that when anemia becomes severer, K wave becomes larger. As blood flow of kidney diminishes in these conditions and in inspiration, we may suppose that augmentation of K wave suggests the diminution of renal blood flow. At least we can assume that K wave is caused not by after-vibration of J wave but by some hemodynamic impulse.

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In previous report it was assured that K wave is caused not by after-Vibration of J wave but some hemodynamic impulse. In this report the author examined what is this impulse, and it was concluded that K wave is caused by the impulse of pulse wave when it, descending the aorta, changes its direction from vertical to horizontal (im my apparatus patients sits on the chair). This conclusion made the calculation of pulse volume at the end of aorta possible. This formula is as follows : Pulse volume at the end of aorta=∫kdt/υ where ∫kdt : area of K wave (gcm/sec) υ : Velocity of Pulse wave (cm/sec) In connection with this, the author referred to the possibility to formulate the relation of blood pressure and velocity of Pulse wave. This formula is as follows : υ=163√(p/ρ) where υ : velocity of Pulse wave (cm/sec) p : blood pressure (cm Hg) ρ : specific gravity of blood

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A statistical study was made on the patients with various types of hypertension who were admitted to Maekawa Clinic from 1946 to 1955, consisting of 99 cases with essential hypertension, 31 with hypertensive glomerulonephritis, 3 with hypertension in endocrine disease and 2 with Kimmelstiel-Wilson's syndrome.The results were as follows.1) Since 1950, the numbers of hospitalized patient with essential hypertension have tended to increase, year by year, and recently also with normotensive glomerulonephritis, but there has been no tendency to increase in those with hypertensive glomerulonephritis.2) Refering to the age distribution, many of patients with essential hypertension, with hypertensive glomerulonephritis and with normotensive glomerulonephritis belonged to 5 th to 7 th, 4 th to 6 th and 3 rd to 4 th decade respectively.3) Judging from the grade of hypertension and Keith-Wagener, most of patients with essential hypertension are considered to belong to slightly or moderately serve hypertensive diseases.4) Electrocardiographic findings in many patients with essential hypertension and hypertensive glomerulonephritis were left axis deviation, left ventricular hypertrophy or changes of ST segments and T waves, but in most of patients with normotensive glomerulonephritis normal pattern.5) Mean values of various renal clearances in these patients were found to be decreased in the order of renal hypertension, normotensive glomerulonephritis and essential hypertension.6) Anemia was one of the characteristic features in the nephritic patients regardless having hypertension or not, whereas in patients with essential hypertension it was not. Electrophoretical studies of sera revealed no characteristic pattern in patients with essential hypertension, but abnormal patterns, especially decrease in the value of total protein and albumin in glomerulonephritic patients with marked albuminuria.7) There were nearly reciprocal correlations between the blood pressure level and K-W grade, between the decrease of RBF value and electrocardiographic changes, between the K-W grade and electrocardiographic changes in patients with essential hypertension or renal hypertension; between the decrease of RBF value and height of blood pressure, between the decrease of various renal clearance values and K-W grade in those with essential hypertension.8) As to the complications at the time of admission of these patients with essential hypertension, cardiac failure or coronary disease was seen in 24% of patients, and hypertensive encephalopathy was in 31.8%. The causes of death among these patients could be sought in aggravation of these complication. As one of the other complications, neurocirculatory asthenia-like symptom was seen in 29.5%.9) In the patients with essential hypertension, the more abnormalities in eyeground, RBF and electocareiogram were there, the worse prognosis was observed.10) It was observed that the patients with slight or moderate essential hypertension responded well to all possible therapeutical procedures as far as various clinical findings and prognosis are concerned, but in patient with severe hypertension no response was observed.

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III) NEUROGENIC HYPERTENSION The neurogenic factor plays an important but not decisive role in the development of hypertension. I have never observed the pure neurogenic hypertension and therefore, I attempted to examine how much role neurogenic foctor plays in various kinds of hypertensions, especially in essential hypertension. For the purpose, I used hexamethonium, 1-hydrazinophthalazine, Rauwolfia Serpentina and phenobarbital.a) 1-Hydrazinophthalazine (Apresoline) : The effects of Apresoline on the renal hemodynamics and blood pressure were observed in 14 hypertensive patients and 1 normotensive ; doses of 0.4 mg/kg, subcutaneously injected. After injection, a reduction of arterial pressure occurred in all cases and this began to develop within 10 minutes and was restored in about 1-2 hours. Then, a slight increase of pulse rate, marked increase of renal blood flow and reduction of filtration fraction were found in 14 cases.Apresoline was orally administered continuously to 7 hospitalized patients (6 with essential hypertension and 1 with chronic glomerulonephritis) and gave favorable results in 6 patients except one patients with nephritis.b) Hexamethonium Bitartarate : By intravenous injection, renal blood flow decreased paralleling with lowering of arterial pressure initially and then returned to approximately control value despite more lowering of blood pressure.c) Rauwolfia Serpentina (Serpasil) : Cardiac and renal functions of 10 hypertensive patients (8 essential and 2 renal hypertensive) were observed before and after single intravenous injection of Serpasil (1-3mg). Reduction of systolic pressure (20-30mmHg) occurred in 7 patients and its maximum existed within 1-3 hours after injection in 6 cases and other 3 cases showed rapid reduction within 15 minutes without latent time. Renal blood flow increased moderately 5 in cases, no changes in 3 cases and decreased slightly in 2 cases. Filtration fraction did not show consistent changes.In oral administration, renal functions showed the similar tendency.d) Phenobarbital : If phenobarbital is administered in nervous patients with hypertension, renal vasospasm would decrease and renal blood flow would increase. I observed in 7 patients (5 with essential hypertension and 2 renal hypertension) changes of renal hemodynamics before and after single subcutaneous injection of 0.1 gm and oral administration of 0.1 gm. In 5 patients with essential hypertension, renal blood flow increased but filtration fraction was unchanged.Next, effects of lumbal puncture on renal hemodynamics were observed. With reduction of cerebrospinal fluid pressure decreased, renal blood flow and glomerular filtration rate decreased and filtration fraction was unchanged.

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