Titlebook: Vasodilators in Chronic Heart Failure; H. Just,W.-D. Bussmann Book 1983 Springer-Verlag Berlin Heidelberg 1983 Dilatation.Failure.circulat

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Prazosin Therapy in Severe Chronic Congestive Heart Failures with acute myocardial infarction and heart failure (1, 2, 3). For long-term treatment in chronic heart failure, however, the number of different drugs is reduced. Oral application and a prolonged action over several hours are necessary, so that nitroglycerin, sodium nitroprusside, and phentolamine

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Early Experience with Captopril in Congestive Heart Failureto be an early phenomenon that abates after sodium retention has led to volume expansion (1). In clinical heart failure, however, activity of the renin-angiotensin system appears to be unrelated to volume status. Plasma renin activity is elevated in some patients who are taking diuretics and in othe

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狂熱語言

Functional and Metabolic Consequences of Chronic Alterations in Preload and Afterload in the Hypertrad (5–8, 13). However, progression of cardiac hypertrophy is a significant precursor of cardiac dilatation and failure and of coronary insufficiency. Therefore, the question has been raised whether specific regression of hypertrophy (14, 15) might be appropriate to prevent both the myocardial and coronary consequences of cardiac hypertrophy.

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遠地點

Nitrates in Chronic Heart Failurertensive crisis concomitant with heart failure, and certain types of cardiogenic shock. Isosorbide dinitrate and nitroglycerin have been investigated extensively. Their actions will be reviewed briefly.

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Endogenous Catecholamines Under Chronic Vasodilator Treatmentthe elevated plasma level of noradrenaline, together with an activation of the renin-angiotensin-aldosterone system leads to an increased stiffness of the arteriolar wall due to salt and water retention. This results in an elevation of peripheral resistance to restore an adaequate perfusion pressure of the vital organs.

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Effects of Hydralazine and Isosorbide Dinitrate on Vasoconstrictor Mechanisms in Patients with Heartthe sympathetic nervous system, on the renin — angiotensin system, and on vasopressin release in patients with congestive heart failure. In particular, we have assessed whether increased activity of these vasoconstrictor systems may limit the drug-mediated effects in these patients.