In 13 patients with various heart diseases, the acute effects of digitalis on the left ventricular performance were studied by the transseptal left heart catheterization using external monitoring of radioisotope dilution and following results were obtained:
(1) In patients with mitral stenosis, in whom heart rate was not altered after digitalization, the cardiac output did not increase significantly presumably because of mitral obstruction, while the left ventricular end-diastolic pressure and volume decreased. This may be interpreted as a result of positive inotropic effect of digitalis.
(2) In patients with mitral stenosis, in whom heart rate was decreased, cardiac output increased significantly in association with an increase of left ventricular end-diastolic pressure and volume. This may be interpreted as a result of negative chronotropic effect of digitalis; that is increased left ventricular filling secondary to increased diastolic filling period.
(3) In patints with aortic stenosis, left ventricular systolic and enddiastolic pressure and volume and systolic tension increased with decrease of left ventricular circumferential shortening rate. This may be interpreted as a result of increased resistance at the aortic ostium and increased contractility of the left ventricle.
These effects of digitalis were compared with those of theophylline ethylenediamine and induced hypervolemia. It is concluded that the modes of action of digitalis on left ventricular function are multiple depending on the state of the heart, and that the effects may generally be expressed as the summation of positive inotropic and negative chronotropic effect.

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Patho-anatomical study was carried on 5 cases with "silent" mitral stenosis to search any responsible factors for a disappearance of pathognomonic apical diastolic rumble.
Compared with 15 control cases with mitral stenosis, the following pathoanatomical determinants were thought to be responsible.
(1) Marked restriction of mitral valve movement, especially of mobile "trigone" of anterior leaflet.
(2) Adhesion, thickening and shortening of chordae tendineae causing the formation of the second point of stenosis below the valve.
(3) Postero-medially deviated mitral valve orifice.
(4) Left atrial huge thrombi.
(5) Combination of these factors.
The meaning of these patho-anatomical factors was discussed.

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(1) Out of 415 autopsied cases in Yokufukai Hospital (old people's home) during last 4 years, 28 cases were given the pathological diagnosis of pulmonary heart diseases: 23 cases of pulmonary emphysema, 3 cases of pulmonary tuberculosis, 1 case of pulmonary fibrosis and 1 case of pulmonary embolism. Although the incidence of pulmonary emphysema is much greater in men than in women, no marked sex difference was found in the incidence of pulmonary heart disease among patients with pulmonary emphysema, pulmonary heart disease occurring in about 20% regardless of the sex. In pulmonary tuberculosis, pulmonary heart disease is seen only in far advanced cases with long standing history.
(2) Pulmonary atherosclerosis in the major arteries and thickening of the intima and media throughout the arterioles, muscular arteries and elastic arteries of the pulmonary vessels were very common in pulmonary heart disease. Histological examination of the pulmonary arterial wall in these cases revealed intimal fibrosis and increase of elastica in the media in the muscular pulmonary arteries. These changes probably represent secondary manifestations of the disturbances in pulmonary circulation.
(3) The aetiologic factors in the production of right heart hypertrophy in several lung diseases have been studied by standard histological methods and by post-mortem pulmonary arteriography. In the cases of pulmonary tumor emboli, primary pulmonary hypertension, pulmonary scleroderma and pulmonary tuberculosis, a marked reduction was observed in the vascular cross section due to obliteration or narrowing in a sufficient extent to raise the pulmonary arterial pressure.
(4) Marked decrease in the number of the small branches of pulmonary arteries was found in the arteriograms in every type of pulmonary emphysema, although the mode of destruction of the arteries is different between the centrilobular and panacinar types of emphysema; in the centrilobular emphysema the central part of the lobule is destroyed while in the panacinar emphysema the destruction is mainly seen in the peripheral part of the lobule. No marked difference, however, was found in the rate of the development of pulmonary heart disease between these 2 types of emphysema. The most important organic changes to reduce the large reserve of the vascular bed of the lung in emphysema appears to be the loss of the pulmonary vascular bed.

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(1) Cardiovascular reactivity, 16 to 28 hours after bilateral nephrectomy was determined in rats by obtaining the dose-blood pressure-response curve in order to avoid the vertical bias.
(2) Bilateral nephrectomy did not increase cardiovascular reactivity to pressor agents (angiotensin and norepinephrine) in rats anesthetized by pentobarbital or anesthetized and treated by pentolinium, a ganglion blocking agent.
(3) In pithed animals without anesthesia nephrectomy augmented slightly but definitely the response to pressor agents.
(4) Further elimination of the neural innervation in pithed animals by administration of bretylium, an adrenergic neurone blocking agent, atropine, and pentolinium, also resulted in an increased response to angiotensin after bilateral nephrectomy.
(5) But it is inadequate to explain the marked augmentation of response to renin after nephrectomy only by the slight increase in response to angiotensin. Response to renin was markedly augmented in pithed animals as well as under usual condition.
(6) Bilateral nephrectomy diminished cardiovascular reactivity to depressor agents (acetylcholine, adenosine triphosphate and histamine).
(7) Angiotensinogen in the plasma increased 4 times more after bilateral nephrectomy. This is the main cause of marked augmentation in response to renin.
(8) The claim that, if angiotensinogen is already in excess, a further increase in its concentration would not lead to an increased production of angiotensin was denied experimentally and theoretically.

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(1) A total of 19 canine kidneys were perfused in situ with the donor's blood or with PVP solution to demonstrate the presence of autoregulation of renal circulation and to investigate the mechanism of it.
(2) The rate of renal blood flow was measured at various levels of perfusion pressure. The rate of renal blood flow was increased proportionately less than the rise in perfusion pressure within a range of approximately 70-200mm.Hg both in innervated and denervated kidneys. This pressure-flow regulation was not deteriorated by the infused dibenamine hydrochloride or regitine inactivating catecholamine, but it was completely abolished by the administration of papaverine hydrochloride, a known direct smooth muscle relaxant. Thus, the presence of autoregulation of renal circulation, the mechanism of which being ascribed to the myogenic nature of the renal vasculature, was demonstrated.
(3) Transient change in renal blood flow after the sudden release of arterial occlusion was composed of the initial sharp rise followed by the rapid reduction towards the control value. The time interval for this response was within several seconds. The rapid reduction following the initial sharp rise in renal blood flow disappeared during the papaverine administration. These findings provided a further support for the active myogenic process of intrarenal vasculature as a causal factor of autoregulation.
(4) During the perfusion with PVP solution, autoregulation was not evident. This is probably due to the damage of renal vasculature by the agent.
(5) During the direct infusion of high concentration of norepinephrine, renal blood flow was reduced to subnormal value and autoregulation disappeared. This fact suggests that autoregulation is not a participant of maintaining sufficient renal blood flow in circulatory emergency which being intensely influenced by humoral factors.
(6) In some kidneys, the effect of elevated venous pressure on renal circulation was studied. Reduction of arterio-venous pressure difference solely produced by elevation of venous pressure was also accompanied by decrease in resistance. It is therefore suggested that the mechanism of autoregulation is related to the arterio-venous pressure difference rather than to the absolute level of arterial pressure.

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Complete A-V block was observed in 18.4 per cent of 38 dogs with the anterior septal artery ligation and in 56.5 per cent of 23 dogs in which both anterior and posterior septal arteries were ligated. No complete A-V block appeared when only the posterior septal artery was ligated.
In dogs which survived one day or more, A-V conduction disturbances were mostly transient even when both anterior and posterior septal arteries were ligated.
Marked histological changes of the A-V conduction tissue were observed in dogs which had suffered from complete A-V block even after normal sinus rhythm was restored.
The results of this study indicate that a rather small part of the crosssectional area of the A-V conduction tissue can carry impulses from the atrium to the ventricle in normal way.

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Pulmonary scintiscanning with I¹³¹ macroaggregated albumin was performed on the first case of abnormal transradiancy of unilateral lung (Macleod's syndrome) found in Japan. It revealed almost complete absence of pulmonary arterial blood flow to the affected lung. We think this method will be of use to clarify the mechanism of this syndrome.

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Forty-three cases of idiopathic dilatation of the pulmonary artery which have been diagnosed clinically by means of the cardiac catheterization are collected from the English literature and their chief clinical features are summarized. A case of idiopathic dilatation of the pulmonary artery with pulmonary regurgitation is presented. The diagnosis of this anomaly is discussed and differentiation of this benign condition from other cardiac lesions is emphasized.

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