The role of hypothalamo-sympathetic nerve system to maintain high blood pressure in DOCA hypertensive rats.
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Biomedical subjects
Publications and source records attributed to H Ijichi.
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Cardiac lesions induced in rats by isoproterenol, a potent beta-agonist, and by repeated stress of restraint and water immersion, in which sensitization of beta-adrenergic receptors would be expected to be induced, were investigated morphologically and following facts were revealed. 1) Cardiac lesions induced by isoproterenol, characteristic findings of which were myocardial hypertrophy, myocardial degeneration and myocardial necrosis replaced by interstitial fibrosis, were more analogous to cardiomyopathy than myocardial infarction or cardiac hypertrophy. 2) Cardiac lesions induced by repeated stress of restraint and water immersion, characteristic findings of which were myocardial hypertrophy, myocardial degeneration and myocardial necrosis replaced by interstitial fibrosis, were similar to those induced by isoproterenol. These results suggest that the endogenously induced dominant beta-adrenergic stimulating action during stress may play an important role in the pathogenesis of cardiomyopathy, the specific etiology of which is not yet known.
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The atrial myocardium has been barely visible with thallium-201 myocardial scintigraphy. This is probably related to the difference in size, distance from anterior chest wall, and small coronary blood flow of the atrium, compared with the ventricle. We have encountered eight cases of visualization of the right atrial appendix (RAA). All had disease involving the right side of the heart, such as mitral stenosis (four cases), congenital heart disease (two), cor pulmonale (one), and primary myocardial disease (one). The RAA was identified from multiple projections in all cases and sometimes confirmed by radionuclide angiocardiography. The RAA was seen at the right upper aspect of the ventricles and was distinguishable from them. Evidence derived from ECG, chest radiographs, and cardiac catheterization, indicated that the most important factor in the visualization might be the displacement of the RAA to a more anterior position.
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In order to establish a new echocardiographic index of the severity of mitral stenosis, left ventricular echocardiograms were digitised using manual tracing and a computer. The instantaneous left ventricular dimension was measured in 15 patients with mitral stenosis. The peak rate of change of left ventricular dimension (peak dD/dt) and the normalised peak rate (peak dD/dt/D) during early diastole were significantly lower in mitral stenosis than in normal subjects. Also, the time between the second heart sound and peak dD/dt was significantly shorter in patients with mitral stenosis than in normal subjects. Correlation between the mitral valve area calculated from the Gorlin formula and peak dD/dt/D was good, while valve area was poorly correlated with the EF slope of the anterior mitral leaflet echo. It is suggested that by continuous measurement of left ventricular dimension and of its first derivative, the reduced atrioventricular blood flow in mitral stenosis can be shown, and that peak dD/dt/D during early diastole is a possible index of its severity.
The effect of prostaglandin E1 (PGE1) on plasma renin activity (PRA) and plasma aldosterone concentration (PAC) was studied in the hypertensive subjects treated with or without 75 mg indomethacin or 60 mg propranolol for a week. Subsequent to the treatment with indomethacin for a week, PRA and PAC levels were decreased as compared to the control, without changes in the blood pressure and heart rate. During the infusion of PGE1, the blood pressure was decreased and the pulse rate was increased. PRA and PAC levels were also elevated. These changes of parameters were not different between the control and the indomethacin-treated subjects. PRA and PAC were suppressed after the treatment with propranolol. With the infusion of PGE1, the level of PRA was not significantly elevated, while, PAC was significantly increased by the infusion of 100 ng/Kg/min of PGE1. During the infusion of PGE1, the blood pressure was decreased while the pulse rate was increased in the subjects treated with propranolol. However, the elevation of the pulse rate was less remarkable than the control. These data indicate that PGE1 have important roles in the regulation of the release of renin and aldosterone. These findings also suggest that PGE1 may act to stimulate the secretion of aldosterone in man.
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The present paper describes the detection of an autoantibody for glutamic pyruvic transaminase (GPT) in sera of patients with chronic hepatic disorders. In 16 out of 500 patients, the existence of an antibody for pig GPT was demonstrated by the double antibody method, gel filtration and radioimmunoelectrophoresis. The antibody was demonstrated as an immunoglobulin G (IgG) with either polyclonal or monoclonal type (kappa or lambda). The binding portion of IgG with GPT was determined as the fragment Fab, but not Fc of IgG. Because the binding of 125I-pig GPT with the patient's antibody was displaced by human GPT, this antibody may have the characteristic of cross reacting with both pig and human GPT. Although the mechanism of production of the antibody for GPT and the pathological significance of the antibody in chronic hepatic disorders remained obscure, possible inhibition of GPT activity in serum is suggested in the presence of this antibody.
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