Hemodynamic comparison of ergometer exercise with isoproterenol infusion was carried out in normal young and old men, and age associated difference in responses to exercise and isoproterenol was evaluated. Ergometer exercises of 50, 100 and 150 W in young men, averaging 23, 0 years, increased heart rate in linear fashion from 73.8 to 149.2, while stroke index was raised at 50 W and remained at the same level thereafter. The isoproterenol infusion of 0.02 and 0.04 μg/kg/min increased heart rate, stroke index and cardiac index by similar amount to 50 and 100 W of ergometer exercise respectively. Ergometer exercise elevated systolic, diastolic and mean blood pressure linearly, while isoproterenol infusion lowered diastolic and mean blood pressure. In old men, averaging 73.0 years, the tolerable limit of ergometer exercise was 40 W. The increase in heart rate, cardiac index and blood pressure at the comparable work level were by similar amount to the young subjects, indicating the identical hemodynamic responses in young and old men at the same work load. Cardiac index to isoproterenol infusion of 0.02 g/kg/min showed less increase than ergometer exercise of 40 W in the aged. Furthermore, the increase in cardiac index to isoproterenol was less in old than young men, showing a decreased response to beta adrenergic stimulation in the aged.

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Weight of the heart and its various components (muscular and non muscular portions) was measured in 138 specimens. Average heart weight for Indians was comparatively less then that of western population. Difference between the average heart weights for males and females was found to be statistically significant. The heart weight was not influenced by age and body length but by the body built. A statistically significant difference was noticed in emaciated persons. Ventricular weight constituted 50 to 80 percent of the total heart weight. A close correlation between the heart weight and ventricular weight was seen. Ventricular wall thickness did not correlate well with the heart weight.

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Renal tissues from 37 patients with glomerulopathies involving glomerular crescents were investigated using an immunofluorescence technique. Immunohistologic findings revealed two kings of crescents, those with fibrinogen deposits (active), and those without (inactive). The degree of IgG deposition in glomeruli with active crescents was much higher than in glomeruli with inactive crescents in acute glomerulonephritis (AGN) and chronic glomerulonephritis (CGN). Active crescents were observed only in biopsy specimens taken within three months after the onset of acute glomerulonephritis or the acute exacerbation of chronic glomerulonephritis. These findings suggest that in AGN and CGN active crescents occur in an earlier stage of glomerular lesions and a more active stage in the immunological process than inactive crescents. The significance of active crescents in SLE, diabetic nephropathy and nephropathy associated with rheumatic arthritis was not evaluated due to the small number of patients.

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The role of noradrenergic neurons originating from the locus coeruleus (LC) in blood pressure regulation was studied by stereotaxic administration of 6-hydroxydopamine (6-OHDA) into the LC in Wistar-Kyoto rats. The administration of 6-OHDA (12μg/6 μl) into the bilateral LC resulted in hypertension and tachycardia, which lasted for 12 days and gradually returned to the levels observed before administration. The systolic blood pressure and heart rate were 172 mmHg and 460 beats/min on the mean respectively, one day after administration. The induced hypertension and tachycardia were closely correlated with the depletion of norepinephrine (NE) content in the cortex and the medulla-pons in rats in a hypertensive state. The correlation between the NE content of the cortex and blood pressure was particularly marked (r = -0.793, p < 0.02). Furthermore, destructive change of the LC was observed histologically in the hypertensive rats. The hypertension was completely prevented by pretreatment with desipramine before 6-OHDA administration. These findings suggest that 6-OHDA induced degeneration, probably mainly in the dorsal bundle originating from the LC and in the LC itself. It is suggested, therefore, that localized chemical degeneration of the bilateral LC causes hypertension and tachycardia as a consequence of denervation of the dorsal bundle of noradrenergic neurons originating from the LC.

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The hemodynamic effects of daily treadmill exercise were evaluated in hamsters with experimental thiamine deficiency to test the hypothesis that increased energy consumption might be a contributory factor in the pathogenesis of beriberi heart disease. Daily exercise enhanced thiamine deficiency and was manifested by earlier development of symptoms of neuropathy compared to non-exercised amimals. Hemodynamics of exercised thiamine deficient animals were characterized by significantly lower O₂ consumption, lower cardiac output, and lower left ventricular minute work, compared to exercised, pair-fed control animals. Left ventricular end-diastolic pressure was slightly but not significantly higher in thiamine deficient animals. Left ventricular function, therefore, was depressed in this group. There was no evidence of hyperkinetic circulation, cardiomegaly or congestive heart failure. Neuropathy and depressed ventricular function, characteristic of pure thiamine deficiency, were observed in the absence of high cardiac output or high output failure, the pathogenesis of which may require other unknown factors.

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Eighteen patients with mitral stenosis and twelve patients with left-to-right shunts heart disease and six normal subjects were catheterized and plasma dopamine-β-hydroxylase (DBH) activities in various parts of cardiovascular system were measured in order to assess the role of sympathetic activity in pulmonary hypertension. Arteriovenous differences of DBH activities were positive in normal subjects and patients with normal pulmonary artery pressure. A negative difference was found in patients with pulmonary hypertension. DBH activity in patients with pulmonary hypertension was significantly elevated compared with that of normal subjects. There was a weak correlation between mean pulmonary artery pressure and DBH activity in pulmonary artery. There were significant differences between normal, mitral stenosis with pulmonary hypertension and left-to-right shunts heart diseases about the pattern of distribution of DBH activity among these groups. A significant difference of the distribution between mitral stenosis with normal pulmonary artery pressure and that with pulmonary hypertension was also found. These findings suggested that a prolonged, increased level of sympathetic nervous system activity among patients with mitral stenosis and left-to-right shunt heart disease developed pulmonary hypertension. Thus, a significant contribution of sympathetic nervous activity to the establishment of pulmonary hypertension was suggested.

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The relations between mechanocardiographic measurements, types of chronic glomerulonephritis (CGN) and clinical data were examined in 70 cases of CGN (20 cases of the latent type, 6 cases of the nephritic type, 14 cases of the nephrotic type, 10 cases of the hypertensive type and 20 cases of the endstage). (1) In the different types of CGN, mechanocardiographic abnormalities increased in the order : latent type < nephritic type < nephrotic type < hypertensive type < endstage. (2) In the endstage, prolongations of ICT, ICT₂ and PEP (p < 0.01), shortening of LVET (p < 0.05) and decrease of LVET/PEP (p <0.01) were observed. These abnormalities may be related to decreased myocardial contractility. (3) Analysis of the relations between mechanocardiographic measurements and results of various tests in all the cases showed that ICT, ICT₂ and PEP were most nearly related to GFR, DBP, γ-globulin and serum sodium and Q-T, Q-II/Q-T and (Q-T)-(Q-II) were nearly related to Ht and age. The changes in cardiac function may be entirely due to increased blood pressure, decreased renal function, electrolyte disturbance, dysproteinemia and anemia associated with CGN. Abnormality in cardiac function seems to depend on the relative abnormalities of these factors and the extents of their influences.

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Fine fibrillar structures could be observed in the peripheral cytoplasm of non-glycerinated mesangial cells. And similar structures were also observed in the peripheral cytoplasm of the cell body of the non-glycerinated glomerular epithelial cells, as well as at the primary processes and secondary processes which were so-called foot ones. In the glycerol treated cells, it was found that the linear thin filaments (50-70 Å in diameter) with parallel arrangement and the rod shaped thick ones (120-130 Å in diameter, 0.15 μm in mean length) parallel to each other, tapering at both sides were located similarly in the case of non-glycerinated mesangial cells. The fibrillar structures in non-glycerinated glomerular epithelial cells were found also in glycerinated ones. In a higher magnification of figures in glycerinated ones, many linear thin filaments (50-70 Å in diameter) with parallel arrangement were found at the location where the similar filaments had been detected in non-glycerinated glomerular epithelial cells, and spindle shaped thick filaments (130-200, 0.14m in mean length) oriented randomly were observed scattering in the peripheral cytoplasm of the cell body and primary processes but not in the foot processes of the epithelial cells. The thin filaments in the two kinds of cells were found to form arrow head structures (HMM-THIN FILAMENTS COMPLEX) in response to the addition of skeletal HMM, which is observable in the filaments of F-actin and those containing actin in various non-muscular cells. The morphological characteristics of rod shaped thick filaments in glycerinated mesangial cells were similar to those of filaments containing myosin from muscles, and the characteristics of spindle shaped thick ones in glycerinated glomerular epithelial cells were similar to those of filaments containing myosin from various non-muscular cells. These thin and thick filaments were thought to be correspondent to myofibrils in muscles.

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Fourteen patients with SVAS served as subjects of echocardiographical and angiocardiographical studies and the data obtained were compared. There were significant decreases in aortic diameter at the level of ascending aorta compared to those of the aortic leaflets and significant differences of the percentage change of the aorta between the patients with SVAS and the normals. Echocardiography is, therefore, a useful noninvasive method for evaluating SVAS. If the values of percentage change of the aortic diameter obtained by echocardiogram are below -30%, the values of peak systolic pressure gradients across the supravalvular stenotic region should be higher tan 20 mmHg. The value of LV M/V under 1.0 suggest than the pressure gradient is lower than 20 mmHg.

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