Relationship between the electrolyte patterns in aorta, heart and serum, and the progression of hypertension in spontaneously hypertensive rat was studied. No significant differences in sodium, potassium and water contents in the tissues, and in electrolyte concentrations in the serum were found between the hypertensive rats at pre- or early-hypertensive phase and control rats of same ages. However, a marked increase in electrolyte and water contents in aorta and a decrease in concentration of potassium in the serum were observed in the hypertensive rats at the advanced phases. These results suggest that the disturbances in tissue electrolytes are not participant of the pathogenesis but of the marked progression of the hypertension.

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The effects of coronary vasodilators, papaverine, iproveratril, dipyridamole and carbochromene on myocardium and coronary vessels and their resultant effects on systemic circulation were studied. Coronary flow, aortic pressure, cardiac output and cardiac work were determined before and after intracoronary administration of the drugs in the anesthetized open chest dogs continuously using electromanometer and electromagnetic flowmeter. Each drug caused characteristic increase in coronary flow. Papaverine, iproveratril and carbochromene caused transient fall in aortic pressure. Iproveratril and carbochromene decreased and dipyridamole increased cardiac output significantly. Papaverine caused some decrease. Iproveratril decreased and dipyridamole increased cardiac work significantly. Papaverine and carbochromene caused some decrease.

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Mitral regurgitation was produced in experimental dogs by cutting the chorda tendinea. The biplane angiography was applied to follow up the geometrical response of the left ventricle to the increased volume overload. The left ventricular cavity volume had continued increasing since the onset of cardiac defects to make up for the diminished effective stroke volume by increasing the total stroke volume which had been achieved without any significant change in the ejection fraction. The end-diastolic pressure which had been elevated soon after the beginning of mitral regurgitation, was shown to be reduced after a sufficient time had elapsed as a consequence of the increased compliance of the left ventricular wall with the development of a muscular hypertrophy. The hypertrophy was evidenced by the regain in the thickness of the left ventricular wall, and the initial stress was shown to be de-creased in consequence. The peak stress was not changed in any consistent fashion but it revealed the tendency to be more elevated when the distension was more marked. These observation suggested that the distension of the ventricular wall should be the primary stimulus for cardiac hypertrophy. The inotropic intervension of the cardiac performance was almost the same in both the normal and diseased hearts. The more rapid velocity of contraction and greater extent of shortening was attained by the contraction originating from the smaller end-diastolic volume with the smaller mural force. These findings form a striking contrast with those observed following the rupture of chorda tendinea and it was indicated that the regulation of the cardiac function following the onset of the acute volume overload depended primarily on the mechanical factor rather than neurohumoral. The augmentation of cardiac output was attained by the increase in the heart rate with an almost unchanged stroke volume. In those with mitral incompetence, the regurgitation was significantly suppressed by isoproterenol. These data suggest the clinical usefulness of this drug in the treatment of acute heart failure due to mitral regurgitation.

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Ventricular irregularities and their relations to collateral circulation were studied on acute occlu-sion of the left anterior descending coronary artery of do, g, heart. The size of the collateral circula-tion existing in normal hearts was estimated by measuring retrograde pressure and blood flow from the occluded artery. Two essentially different types of ventricular arrhythmias were observed in the early and later stages after acute occlu-sion. The mortality in the early stage resulting from ventricular fibrillation was 39.5%. The frequency of extrasystole in this stage was inversely related to the magnitude of collateral circulation. The arrhythmia in the later stage disappeared and reverted to regular sinus rhythm during a period of backward bleeding for measuring retrograde flow. The backward bleeding not only brought back a regular rhythm, but also improved left ventricular performance. Some arrhythmogenic substances originated from ischemic tissue probably take part in the genesis of the arrhythmia in the later stage.

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On a total of 130 cases, including 36 normal cases and 94 cases of various diseases, consisting mainly of 36 cases of hypertension, esophageal phonocardiography (PCG) and precordial PCG were performed to observe normal and pathologic atrial sounds. At the same time, the relation to ECG findings, systemic blood pressure and pulmonary pressure obtained by right heart catheterization was observed. Then the rate of appearance of atrial sounds by esophageal PCG and precordial PCG and their nature were compared and reviewed and correlations to the severity were obtained. Also various loading tests were performed on the same cases of hypertension to review changes in atrial sounds. Atrial sounds recorded by esophageal PCG are generally larger in intensity than those recorded by precordial PCG and the rate of recording atrial sounds by the former method was 114 cases (88%) of all the 130 subjects, 30 cases (82%) of the 36 normal cases and 36 cases (100%) of the 36 cases of hypertension. On the other hand, atrial sounds were recorded by precordial PCG in 40% of all the subjects, 25% of the normal group and 58% of the hypertension group. Atrial sounds were frequently recorded by precordial PCG in cases of left ventricular hypertrophy and ST, T abnormalities on ECG. The rate of recording atrial sounds by precordial PCG was high in cases of hypertension and left ventricular hypertrophy, namely, cases with large left ventricular overloading. Further for such cases, there was a relative tendency of shortened P-IV interval on PCG as against P-R interval on ECG. These changes in P-IV interval were also noted in cold pressor test, Valsalva's test and amyl nitrite inhalation test performed on the same case of hypertension. It was presumed that atrial sounds (2nd component) were dependent upon left ventricular overloading. Pathologic atrial sounds recorded by esophageal PCG and precordial PCG were compared with atrial sounds of normal cases, which revealed that atrial sounds recorded by precordial PCG were considered to be atrial sounds which became large in intensity (or had pathologic elements) and were conveyed to the chest wall. However, there were some cases with more possibility of pathologic findings, which were recorded by esophageal PCG but not by precordial PCG. Even in these cases, differences of P-R : P-IV were large and from the aspect of timing, it is possible to some extent to predict latent heart insufficiency. In this meaning, the clinical value of esophageal PCG is very large.

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