IN the past decade since Knipping introduced radioactive rare gas for the study of regional pulmonary function, advantages of the radioisotope method over conventional methods were soon recognized and various methods were developed. These new methods enabled more precise study of overall gas exchange in the whole lung.
Relationship between the regional distribution of blood flow and that of ventilation is of great importance because inequality of these two functions is now considered to be one of the main causes of hypoxemia in medical cases.
Therefore, 52 cases with chronic cardiopulmonary disorders were studied to find the final functional state of regional ventilation-perfusion relationship in pulmonary lesions which began from either predominant ventilation or perfusion disturbance. To this end, the radioactive rare gas method reported by Dollery et al. and the scanning method by Drs. Taplin and Wagner were performed. At present authors are using both of these methods. The results obtained by the rare gas method were reported in this article.

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WITHIN the recent decade, distinguished advancement has been made in application of ultrasound in various medical fields. Ultrasonic technique can realize images of the soft tissues by both absorption and reflection, which structure is more clearly identified with this technique than with X-ray in a fine contrast due to different propagation constants of ultrasound between tissues. A number of investigators have focused their efforts on visualization of the soft tissue structure and its movement by various pulse-reflection methods. These methods have been proved of a great diagnostic value and have appeared to be promising to the future.
One of the advantages of ultrasonic diagnosis is absence of pain and diagnostic surgery. However, if a little surgery is added, application of this diagnostic method is extended. As for application to the heart, conventional ultrasonic echography through the chest wall is limited in indication and in result, being disturbed by precardiac tissues as well as air in the lung.
In 1960, Cieszynski reported the intracardiac method with a miniature ultrasonic probe inserted into the heart lumen through the jugular vein of an anesthetized dog and he obtained reflections of ultrasound from the surface of the right and left heart lumen as well as from the great vessels without any harm.
Since 1962, the author devised and applied the ultrasonic intravenous probe to animals and patients with heart diseases, which is called the “cardiac sonde” while another probe for detecting liver lesions is called the “liversonde” which was introduced in our previous papers.
In this paper, principle, procedures and results of the intracardiac ultrasonic scanning inside the heart with this probe are described with a focus in detection of atrial septal defect of the heart.

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The importance of correction of acid-base derangement for the care of surgical patient has been stressed recently. Despite of intensive study of the hemodynamic aspects of its derangement, these results were not entirely consistent. Accordingly, evaluations were made concerning the influence of metabolic acidosis and its correction on myocardial performance and vascular resistance in dogs and clinically the effectiveness of correction of metabolic acidosis on myocardial contractility after an openheart surgery. The result indicated that metabolic acidosis had a considerably adverse effect on the myocardium and the peripheral circulation, and that correction of metabolic acidosis was quite beneficial to restore cardiovascular dynamics.

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The mechanism of the reflex depressor function from the kidney was studied in anesthetized dogs with penthobarbitone sodium under artificial breathing.
The action potentials of the efferent renal nerve (sympathetic) decreased by compression of the kidney and renal vein occlusion, and were followed by a fall in the systemic arterial pressure. The efferent action potentials were slightly increased or unchanged by renal artery occlusion but were followed by a rise in the systemic arterial pressure.
The action potentials of the afferent renal nerve increased with the rise in the intrarenal pressure produced by compression of the kidney, by renal vein occlusion, and by elevation of the perfusion pressure of the kidney in cross-perfusion experiments.
The afferent discharge decreased with the fall in the intrarenal pressure produced by renal artery occlusion. The action potentials of the efferent nerve decreased by electric stimulation of the afferent nerve, and were followed by a fall in the systemic arterial pressure. The action potentials of the afferent nerve evoked by compression of the kidney, by elevation of the intrapelvic pressure, and by renal vein occlusion, did not vanish after subcapsular and intrapelvic injection of 2% procaine or after total decapsulation. The evoked action potentials disappeared after injection of procaine into the renal artery.
It was concluded from these data that the receptor, which is sensitive to the changes of the intrarenal pressure, is activated by elevation of the intrarenal pressure and causes reflex hypotension by means of the inhibition of the sympathetic discharge.

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In order to establish a reliable method for the determination of plasma renin activity in small samples, we have compared the methods reported. The method of Boucher et al. was found to be reliable, and modified in the laboratory. Expression of renin activity by the first order reaction constant was emphasized.

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As far as the counterclockwise frontal loop directed superiorly and to the left is concerned, persistent common atrioventricularc anal is the most common cardiac anomaly encountered. However, there are many lesions other than atrio-ventricular canal which present this peculiar vectorcardiographic pattern. In the present study, vectorcardiograms showing this peculiar pattern of atrial septal defect (ostium secundum type), ventricular septal defect, tetralogy of Fallot, tricuspid atresia, and transposition of the great vessels were analyzed. In addition, several points of prime importance, necessary for differentiation, were emphasized.

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Arare, however, surgically important condition in which both great vessels arise from the right ventricle has been recognized for many years. Witham, 1) applying the term of “double outlet right ventricle” to the anomaly, divided it into two groups clinically at the first time in 1957 : the “Eisenmenger type” without pulmonary stenosis and the “Fallot type” with pulmonary stenosis. The term “origin of both great vessels from the right ventricle” has also been used to define the entity. Since then McGoon2) reported the first case of successful repair in 1961 and was followed by the case of Redo et al.3) which was diagnosed preoperatively and operated upon in May of 1961.
The development of cardilogy and cardiac surgery, and an increasing experiences in cases of tetralogy of Fallot and advanced ventricular septal will be occasionally quite difficult. And from surgical point of view, the recognition of this disease is very important to have it repair correctly even in surgery.
This is an additional case which was clinically very similar to ventricular septal defect with moderate pulmonary hypertension and was found to be the anomaly at surgery.

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REVERSED splitting of the second heart sound has been regarded as the one of the most important phonocardiographic signs in case of complete left bundle branch block (CLBBB), aortic stenosis, patent ductus arteriosus, and others. This type of splitting is called “paradoxical”, because, contrary to a usual respiratory behavior, inspiration causes a “narrowing” of the interval between 2 components, pulmonic (IIP) and aortic (IIA), of the second heart sound.4 In the extreme, the splitting may be abolished duringpost-inspiratory beats. In this sense, “reversed” splitting and “paradoxica” splitting are synonym.
This paper describes a case of reversed splitting without paradoxical respiratory response. Although the true mechanism is still unsolved, the early appearance of “IIP” during post-inspiratory beats has the primary importance in this particular situation, in which the splitting widens on “inspiration”.

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IT is very rare that Adams-Stokes syndrome occurs in hypopotassemia and only 2 cases are reported in the literature.1) These cases were caused by atrioventricular block, though in this case the Adams-Stokes syndrome was caused by ventricular fibrillation that was recurrent, transient and reversible. The patient was, moreover, relieved by potassium chloride. Such a case was not reported yet in the literature as far as we know.
The massive fused T and U wave inversion, the postextrasystolic alteration of it, the alternans of the U wave after the cessation of ventricular fibrillation and the postextrasystolic alteration of the U wave were seen in this case. These were very interesting signs in the electrocardiogram to resolve the ionic shift in the myocardium in these occasions.2) The antiarrhythmic drug of ajmalin was effective in the initial stage in this case, though it became ineffective in the further advanced stage of hypopotassemia. This finding is interesting, if we refer the ineffectiveness of quinidine in hypopotassemia which is shown experimentally.3)
Such a rare case is presented with the review of the literature and the mechanisms are discussed.

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THE orthostatic hypotension in the presence of essential hypertension with the organic changes in the cardiovascular system is only rarely reported. The remarkable fluctuation of the blood pressure in this may be a precipitation factor of myocardial infarction as it was suggested by Dr. Mainzer. The complete postmortem study in this disorder has been reported only in a few cases.
In this case the death was caused by myocardial infarction that seemed to be precipitated by the orthostatic hypotension in the presence of essential hypertension and an autopsy was performed.

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SKELETAL deformities of the thorax are known to produce functional disturbances of the cardiopulmonary system. A number of cases of funnel chest and thoracic kyphoscoliosis have been reported to cause cardiac failure. In this communication we report 2 cases of cardiac murmur caused by the deformity of the thorax due to congenital abnormalities of the spinal column. Case 1 was attributed to a relatively new clinical entity called “straight back syndrome” and Case 2 was a member of a family affected by Morquio Brailsford's disease.

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MOST investigations of pulmonary edema have concentrated either on the initiating factors that lead to excess fluid leakage from the pulmonary capillaries or on the gross pathophysiology of the lung and whole animal. There is an intermediate process which is that of fluid movement and accumulation within the various spaces inside the lung. This process has received very little attention perhaps, as Visscher and his associates stated, due to the lack of good methods for seeing the edema process with precision.
A few direct and indirect studies of individual components of the process have been made such as the electron microscopic studies of Schulz on the thickening of the alveolar septum in edema and the all-or-none filling of individual alveoli deduced from the mechanical behavior of edematous lungs by Cook and co-workers.
In our studies we examined the histologic pattern of fluid filling by using rapid freezing of the inflated, living lung: a procedure that fixes the lung very quickly at a given point in time, thus permitting us to “see” the lung as it was in life.

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THE rate of passage of substance across the capillary wall measured in terms of increased quantity (ds) passing through during a period of time (dt) is directly proportional to the area (A) of the wall, the driving force between the inside (Ci) and the outside (Co) of the capillaries, and the diffusion constant (K) for the substance, and is inversely proportional to the thickness (θ).
ds/dt=A/θ(Ci-Co)
The area of the wall, namely, the area of the pulmonary capillary wall depends on the venous return and pulmonary blood volume, and the driving force is the pressure gradient between the hydrostatic pressure of the pulmonary capillary and the tissue pressure of the lung. These 2 components are variable with the hemodynamic changes.
The thickness of the capillary wall is related to its diameter, depending on the capillary blood volume. So it may be variable not only by the hemodynamic change, but also by the injury due to chemicals, gases and some other physical factors.
The hemodynamic changes related to an increased permeability, such as the elevated pulmonary capillary pressure and increased pulmonary capillary blood volume, may be caused by an increased vasomotor activity elicited by stimulation of the central nervous system by various means.
An increased capillary filtrate is drawn back by the effective osmotic pressure to the capillary distal to the venule to prevent from accumulation of the excessive extracellular fluid.
Some part will be drained through the lymphatic channels to the superior vena cava.
If the pulmonary transudation is increased beyond an attractive force of the effective osmotic pressure to drawn fluid inward, then the lymph flow is bound to be increased.
Lowering of the osmotic pressure as well as obstruction of the lymphatic channels would provide auxiliary factors to retain interstitial fluid.
So far as the lymphatic flow is found to be increased concomitantly with enhanced transudation of the pulmonary capillary, it is reasonably assumed that measurement of the lymph flow can be served as an index of the permeability of the lung capillary.
In this report, attempts have been made to measure the lymph flow of the lung to know the effect of the sympathomimetic drug and anoxia both of which are considered to offer a number of conditions intimately related with development of the pulmonary edema.

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PULMONARY edema has been produced by various agents and methods in experimental animals. Of particular importance to hemodynamic research is the consistent production of an acute pulmonary edema in a fairly large animal which will facilitate necessary determinations. The present report attempts to elucidate some hemodynamic aspects and importance of blood pressure regulation in the development of acute pulmonary edema in the dog.

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THE development of pulmonary edema in heart disease is closely related to the cardiac decompensation. Its fundamental disorder is generally believed to be the intensification of pulmonary congestion due to the cardiac decompensation. This concept, however, depends on the indirect evidences such as clinical symptoms, chest X-ray findings and the measurement of pulmonary vascular pressures and central blood volume.
With the introduction of left heart catheterization by transseptal route, it has become possible to study the dynamics of the left heart with safety and little discomfort to the patient. Utilization of indicator-dilution technique, combined with simultaneous right and transseptal left heart catheterizations, has made it possible to estimate more precise quantitation of pulmonary congestion, i. e., the true pulmonary blood volume and pulmonary circulation time.
The purpose of this presentation is to report the role of heart failure in the pathogenesis of pulmonary congestion and edema in heart disease.

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Filtration patterns from the pulmonary vascular bed into the pleural space differ from those for the airway spaces. In the pleural space, the direction and the rate of filtration are proportional to the vascular-pleural pressure differences. Filtration into the airway is inhibited as long as vascular pressure exceeds airway pressure by less than 12cm. H₂O. At higher transmural pressures filtration is very rapid. Retrograde perfusion produces more filtration than antegrade perfusion. These data suggest that the transmural filtration occurs at the venous end of the capillaries and perhaps in the venules. A special property of the airway prevents filtration until a critical value is achieved. The significance of these filtration patterns in ventilation, effusion and edema are discussed.

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