1) Plasma ADH levels measured by bioassay in the group with extracorporeal circulation were 2.3 ± 0.6 μu/ml before surgery and 6.6 ± 1.8 μu/ml during anesthesia. They increased to 196.5 ± 62.3 μu/ml or about 100 times greater than before surgery during cardiopulmonary bypass. 2) In the group without extracorporeal circulation, plasma ADH levels were 1.5 ± 0.9 μu/ml before surgery and increased to 44.1 ± 15.2 μu/ml during operation. 3) After operation decrease in plasma ADH level was relatively rapid in both groups. It became three times that of the control level in the morning of the next day. 4) Marked increase in plasma ADH level during cardiopulmonary bypass was much the same as it was during hemorrhagic shock in dog experiments. 5) Fall in mean arterial blood pressure and loss of pulsatile blood flow will play main roles in this marked increase in ADH during cardiopulmonary bypass through stimulation of arterial baroreceptors and probably chemoreceptors. 6) In two cases with mitral stenosis, increase in plasma ADH during cardiopulmonary bypass was lesser than the other heart diseases.

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While studying morphological changes in heart 1-3 cm of Aorta was also removed and incidence of atherosclerosis in that portion was studied. In all 110 aortas were examined. Atherosclerotic lesions were observed in 77 aortas (70.0%). The incidence increases with the age and beyond 4th decade all the aortas were affected. Fatty streaks were observed in 2nd decade involving only 7.5% of the total intimal surface and reaching to a maximum of 22.2% in the 3rd decade. Fibrous plaques involved a small area (2.6%) in 3rd decade, followed by a gradual rise to 9.2% in 7th decade. Complicated lesions though occurred in 3rd decade involving 0.7% surface but a maximum coverage (4.5%) was seen in 7th decade. These findings have been discussed in the light of observations of other workers. There is slow progression of fibrous plaques and paucity of complicated lesions in Indians as compared to white population. The study has further revealed that the encrustation of mural thrombi is probably the main basis for the progression of the atheromatous lesion.

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Changes in acid phosphatase activity in the cerebrovascular system and brain parenchyma in SHR were investigated histochemically. An increased activity of the enzyme was demonstrated in the SHR endothelial and medial smooth muscle cells of the cerebral arterial system as compared to the control. The pericytes of intraparenchymal blood vessels also showed an intensified enzyme activity. The enzyme activity increased with advancing age. In SHR brain parenchyma, the enzyme activity was decreased in the cortical nerve cells. Glial cells with the enzyme activity were increased in number and showed an intensified activity. Causative factors of changes in acid phosphatase activity in SHR cerebral arteries and parenchyma were discussed.

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M-mode and cross-sectional echocardiograms were obtained in 30 patients with rheumatic mitral valve disease (24 : MS, 6 : MR) pre and post-operatively for the evaluation of their severity. Echocardiographic findings were compared with operative findings. Mitral valve area (MVA), E-F slope (DDR) and mean circumferential fiber lengthening during rapid filling course (mVcF(RF)) were measured in patients with MS (1.2 cm², 14mm/sec 1.3 circ/sec respectively) and they were significantly improved after operation (2.2 cm², 35mm/sec, 19 circ/sec respectively). Assessment of fusion of both commissures could be detected in 8 of 13 cases (62%) who underwent papillotomy in addition to commissurotomy. In patients with MR, short axis images of cross-sectional echocardiogram showed mitral incompetence during systole with marked enlargement of left atrium and mitral annulus (63 mm, 46 mm respectively). It was suggested that M-mode echocardiogram was more useful to estimate the axial dimensions and the cardiac cycle and was sensitive to detect rheumatic mitral valve disease, but it was of limited valve for the assessment of its severity. On the other hand, cross-sectional echocardiogram was proved to be valuable for the assessment of the whole mitral complex, which was useful not only for the evaluation of the severity of mitral valve disease but for the assignment of operative category.

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Eighty cases with mitral valve prolpase excluding the secondary prolapse of the mitral valve caused by known underlying diseases were studied by real-time ultrasoundcardiotomography and M-mode technic. It was thought that observation of the left ventricle with long axis sector scan was useful and sensitive technic to diagnose the mitral valve prolapse. By comparative study of M-mode technic and ultrasoundcardiotomography, echo sources and the mechanism of so called prolapse patterns such as pansystolic bowing, mid-systolic buckling and multilayered echoes were explained. Pansystolic bowing and mid-systolic buckling were considered as the reliable signs for diagnosis of anterior leaflet prolapse, but were not diagnosis of anterior leaflet prolapse, but were not contributory to diagnose posterior leaflet prolapse and ultrasoundcardiotomographic technic was needed to detect the posterior leaflet prolapse. According to the mode of prolapsing findings by ultrasoundcardiotomograms classification of severity of mitral valve prolapse was undertaken and its grade was expressed as AmPn in which A and P designated prolaspe of the anterior and posterior leaflet respectively and m and n indicated the grade of severity in number from zero to five.

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1)Left ventricular hypertrophy in hypertension is almost symmetric. However, the interventricular septum is slightly thicker than the posterior wall. In aortic regurgitation and mitral regurgitation the posterior wall is thicker than the interventricular septum. The above situation suggests a difference between the influence of pressure overloading to the heart and that of volume overloading. Hypertrophy in congestive cardiomyopathy is similar to that in aortic regurgitation. 2) The interventricular septum was thickened in all the examined cases of hypertrophic cardiomyopathy. In some cases the interventricular septum was mass-like, bulging into the left ventricular cavity and in some cases into the right ventricular cavity. 3) In the posterior wall of the left ventricle, various degrees and extents of hypertrophy are observed, with and without hypertrophy of the papillary muscle. In some cases, only one of the anterolateral and posteromedial papillary muscles is hypertrophied, but not the other. These findings reveal that a nonuniform hypertrophy develops not only in the septum and free wall, but also even in the papillary muscles. In one examined case a muscle bundle was hypertrophied, occupying a large space in the narrow ventricular cavity, but not the papillary muscle. 4) Motion of the hypertrophied ventricle especially the maximum velocity of the thickened posterior wall during rapid filling, is generally slow. There is a trend that the thicker the posterior wall, the slower the maximum velocity in rapid filling. However, the posterior wall velocity in cases of hypertrophic cardiomyopathy in diastole is generally slower than that in cases of hypertensive heart, even if the posterior wall thickness is the same in both conditions. 5) The mitral SAM consists of echoes of the mitral chordae which are shifted forwards by the hypertrophied papillary muscles sticking out anteriorly into the left ventricular cavity in systole. 6) The hypertrophied and maloriented papillary muscles occupying a large space in the narrow cavity possibly play an essential role in developing the intraventricular pressure gradient in cases of hypertrophic obstructive cardiomyopathy. 7) The obstructive and nonobstructive forms of hypertrophic cardiomyopathy do not seem to be essentially different, but with various manifestations, depending upon the locality and extent of nonuniform inappropriate hypertrophy, form a continuum.

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Echocardiography combined with simultaneous measurement of peak systemic pressure was applied for analysis of left ventricular function within a two-dimensional framework which took into account the preload, the afterload and the level of myocardial inotropic state. This approach is particulary useful for understanding the behavior of the normal and diseased ventricle under various abnormal loading conditions where a single measurement of ejection characteristics does not necessarily reflect inotropic state. The pressure (or wall stress) - diameter loops were constructed during systolic pressure change and diameter at the end of ejection was linearly related to systolic pressure or systolic wall stress. This relation generally approximates the isovolumic length- tension relation which is independent of initial length and unique to a given level of inotropic state. The echocardiographically determined shortening velocity of the ventricular wall (mean Vcf) is inversely related to the level of afterload, if the preload is fixed. However, the normal human ventricle exhibits only minor changes in Vcf in response to a moderate acute pressure stress, as modified by the preload (Frank-Starling) reserve. If the limit of preload reserve is reached, Vcf will diminish ; that is, a mismatch between afterload and the level of inotropic state occurs. The echocardiographic approach for the assessment of cardiac performance thus allows an early detection of impairment of ventricular function and offers a possible explanation of how the ventricle operates on a descending limb of function and of how the ventricle adapts to chronic mechanical overload.

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