PATHOPHSIOLOGICAL SIGNIFICANCE OF SYMPATHETIC ACTIVITY IN CARDIOVASCULAR DISEASES
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概要
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On cases with valvular disease, essential hypertension and coronary heart disease, each of which has a cardiac function estimated Class I and Class II according to the functional classification by NYHA, the reactivity of the sympathetic nerve center to the endogenous or exogenous stimulation, and the responses in the cardiovascular system to the induced sympathetic hyperactivity were studied, and the following results are obtained: (A) Valvular disease l. A sympathicotonic state was shown even during the rest, and the reactivity of the sympathetic nerve center to various stimuli was augmented. 2. The responsiveness of a failing heart to CA was normal or lowered. This leads to an increase in the CA secretion as a homeostatic mechnism. 3. Despite the increase in the CA secretion, cardiac output during the exercise was less greatly increased than that in a control. As to the p-blocker administration, the increase in the CA-secretion by the exercise was augmented but that in cardiac output was suppressed conversely by the β-blocker. These facts will mean that CA plays an important role in the regulatory mechanism in a failing heart, limits having been naturally set to its effects. 4. The suppressing effect of the β-blocker on the tachycardia caused by the exercise was not so great as that in a control, in hypertension, or in coronary heart disease. The changes in stroke volume by the exercise were slight, regardless of being pretreated by the β-blocker or not. In a failing heart, pulse rate plays an important role in maintaining the cardiac output. And it will be understood as a compensatory mechanism to maintain the cardiac output that the increase in heart rate by the exercise is not easily suppressed' by the β-blocker. The heavy suppression of the increase in heart rate may, therefore, possibly induce aggravation of heart failure. (B) Essential hypertension 1. The sympathetic activity during the rest was normal, and the responsiveness of the sympathetic nerve center to various stimuli was slightly but insignificantly higher than that in a control. 2. The reactivity of the peripheral vascular system to the exogenous or endogenous sympathetic stimulation was demonstrated greater than that in coronary heart disease as well as than that in a control. 3. The increase in blood pressure by the exercise was suppressed by the β-blocker not so greatly as that in a control or in the other disease groups. 4. The increase in stroke volume by the exercise was suppressed only slightly by the β-blocker. From above, it indicates that the a-receptors in the peripheral vascular beds are on a hypersensitive state, and, furthermore, the sympathoadrenal system may participate greatly in the pathogenesis of essential hypertension. (C) Coronary heart disease 1. The reactivity of the sympathoadrenal system to endogenous or exogenous stimuli was elevated. 2. Augmented hemodynamic responses to CA were demonstrated, and the oxygen-requirement as well as cardiac work was liable to be increased, and even an amount of NA within a physiological range can also cause a similar diseased state to exercise-induced myocardial ischemia. 3. The response of the cardiovascular system to the exercise was suppressed by the β-blocker. These results suggest that the sympathoadrenal system plays an important role in myocardial ischemia and that the β-blocker is of clinical use in preventing an anginal attack. On cases of valvular disease, essential hyper-tension and coronary heart disease, the reactivity of the sympathetic nerve center, and the corresponding changes in the sympathetic activity, as well as the reactivity of the cardiovascular system, were studied. Each of them in one of the three underlying diseases was demonstrated to differ from those in other underlying diseases. Under these observations, as well as the observation on the changes caused by the β-blocker, the differences in pathophysiological significance of the sympatho-adrenal system were also d
- 社団法人日本循環器学会の論文
- 1974-05-20