An investigation of respiration of rat heart muscle slices was carried out using the manometric (Warburg)technique. In this report, the respiration in the presence of glucose and fructose as substrate was studied comparing with that in the absence of added substrates, namely, endogenous respiration. In the study by heart muscle slices, as we know, slight difference of the experimental condition has various influences upon the experimental result. So, I paid consideration to maintain the same condition throughout my experiment. Nevertheless, the respiration rate of the individual slice showed considerable discrepancy, and its causes were discussed. (Fig. 2.8.9.)Results were as follows.1) Qo₂ (gas consumed per mg. initial dry weight/hour) in the endogenous respiration at first hour was 11.4, equal to Qo₂ in the presence of 0.01 M Glucose as substrate. However, it declined rapidly at first, subsequently less markedly, so Qo₂ in the fourth hour became 2.3, being 20 per cent of the initial value. (Fig. 1, Table 1, 2)2) When 0.01 M glucose was added after 1-2 hours, its effect on the respiration was not manifest during the first hour, but slowly thereafter. So, Qo₂ did not continue to decrease, as it did by no addition of substrate, but began to increase little. However, at the end of third hour after addition of glucose, Qo₂ was not higher than the initial value. This result suggests that the speed of glucose utilization by heart muscle slices is very slow. (Fig. 4 Table 3).3) Qo₂ of heart muscle slices in the presence of glucose : When gas was 100 per cent O₂, Qo₂ in 0.01 M glucose-Ringer was 11.4 at first hour, and in 0.02 M glucose it increased to 18.4. In the former, its value was maintained as long as 6-7 hours. In the latter, it decreased little at first hour, but then became constant. (Fig. 3. Table 2) When gas was air, Qo₂ decreased to about 30 per cent of that in pure oxygen, and similarly its initial value did not change during 3-4 hours, disregarding the amount of glucose concentration as 0.01 M or 0.02 M. (Fig 5, Table 4, 5.) After all, glucose was oxidized not so easily and rapidly, but when it was present, the respiration of slices was constant for long hours independently of oxygen tension and of glucose concentration.4) Fructose, one of the common carbohydrates which not infrequently gives rise to discussion comparing with glucose as the important metabolic source, did not increase oxygen uptake of heart muscle slices. Moreover, by the chemical estimation of fructose and fructoseester in medium before and after the manometric experiment, it was indicated that fructose was not consumed at all by heart muscle slices. Even if fructose is worthy of energy source of the heart muscle, as has been mentioned by some groups of workers, the author feels it is reliable that fructose itself does not concern directly with heart muscle metabolism. (Fig. 6.7. Table ct6.7.8.)

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The present study was designed to present microscopic findings of various organs of the rabbits with aortic or pulmonic stenosis. The histological material available for this study consisted of sixty-one rabbits, four of which showed chronic congestive heart failure clinically or at autopsy. The duration of the experiment varied from 15 hr. to 495 days. The summary and conclusion of this study is as follows : 1. As the pathologic changes in the heart, hypertropy, atrophy or degeneration of the muscle fibers and myocardial fibrosis in many rabbits, and myocardial inflammatory lesions in some rabbits were found. But cardiac failure did develop in four rabbits without good correlation with the character, extent, or localization of these cardiac lesions. These pathologic changes were merely evidences of myocardial disease and could not be indicative of cardiac failure. The microscopic study of the heart did not reveal any characteristic lesions qualitatively nor quantitatively which could adequately account for the development of cardiac failure.2. In many rabbits with aortic stenosis the lungs showed venous congestion, edema and thickening of alveolar wall. Cardiac cirrhosis of the liver was found in two rabbits with pulmonic stenosis and partial cirrhosis, in one with aortic stenosis. Fibrosis of the spleen was found in one rabbits with pulmonic stenosis. The kidneys revealed little changes related with cardiac failure, except for a slight venous congestion.3. The results of the visible macroscopic and microscopic study of various organs indicate that the passive venous congestion is localized in the organs retrograde from the failing cardiac chamber and it is more striking in those organs proximal to that chamber, and that this congestion is already present even in the so-called "Stage of Incompensation".

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Although we have never read the report about the correlation between pericarditis and serum protein, often found recently hypoproteinemia in pericarditis patients, and checked sera on 14 cases, admitted into our clinic. 8 cases among them showed low serum protein level.Hypoproteinemic cases were worse in their clinical feature. But primarily euproteinemic cases were well, and cases that original hypoproteinemia was normalized by treatment were well, too.Homburger and Petermann revealed that hypoproteinemia might occur because the circulating blood is inadequately supplied with protein or because too much of it escapes. But the common abnormal factors i. e., pyrexia, oligorexia, altered vascular permeability and cardiac insufficiency are not characteristic in this disease. For example there is no hypoproteinemia in pleurisy that closes to pericarditis pathologically and etiologically. And then by our observation there was little correlation between hypoproteinemia and liver enlargement, edema and pericardial effusion.The mechanism of hypoproteinemia in pericarditis is indifferent from these factors alone, but perhaps influenced by general and severe disorder of protein metabolism.

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Many researches have been done for the analysis of the ventricular activation process by means of extremity lead ECG or unipolar chest lead ECG. But those by means of extremity lead ECG and too rough to discuss the excitation process, and those by means of unipolar lead ECG are too prejudiced. According to our previous report on the relationship between the unipolar lead ECG and VCG, one can analyse the intraventricular activation process far minutely. So tried the analysis of intraventricular excitation process by means of combined use of the unipolar lead ECG and VCG.Method 20 unipolar lead ECG and the lead points of fronatl, horizontal and sagittal planes of Vectorpolyogram by Toyoshima were taken simultaneously with V_F and the electrical potentials at each instant in QRS duration were measured standardizing the main peak of QRS in V_F ECG. From these electrical potentials obtained by measurement, I constructed Vectorpolyograms in three planes, and compared them with those recorded by polyography. When they were coincident very closely each other, they were used for the analysis of intraventricular activation process. Theoretically, the constructed VCG must be coincident with polyograms, but for several reasons, especially for the difficulty of accurate potential measurement of synchronous instant they were not always coincident each other. Materials.The materials were 40 normal adults, 7 patients with ventricular hypertrophy, 4 patients-with bundle branch block, and 1 patient with ventricular premature beat.Results obtained In normal adults, the heart region depolarized at first was subendocardial muscles of either side of the septum, and then those of free walls. The activation in subepicardial muscle began earliest at the anterior aspect of right ventricle and then extended radially. The apical portion was earlier than the basal portion. Activation in subepicardial muscle was not fired after the accomplishment of activation in subendocardial muscle but was fired always on the way of activation of subepicardial muscle. Generally, the subepicardial muscles in diaphragmatic and basal region were activated lastly.The depolarization in the heart with ventricular hypertrophy developed in the order at first, but the influence of the hypertrophied ventricular walls the VCG was recorded in its specific pattern, and the last portion of the activation was the posterolateral subepicardial muscle at the hypertrophied wall.In the heart with bundle branch block, the subednocardial muscles of the septum and of the anterior free wall at the intact side were activated in the first and then the subepicardial musles of the same side. The depolarization of the subendocardial musle of the posterior free wall of the block side began to depolarize about this time and extend gradually to anterior. The subepicardial muscle depolarized in order of back to front and apparent delay of inscription of QRS loop was marked in this period. The occurrence of this delay was the difference of b. b. b. from hypertrophy of ventricle.In the case of ventricular premature beat of right ventricular origin, the activation of the right ventricle was earlier than that of the left ventricle, and the order of affection in the left ventricle, differing from that in the left bundle branch block, was nearly the same with that in normal heart. Namely from the anterior to the posterior and from the apex to the base.

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