The Effect of Beta Adrenergic Blockade on Patterns of Urinary Sodium Excretion
Studies in Normal Subjects and in Patients with Heart Disease
- STEPHEN E. EPSTEIN, M.D.; and
- EUGENE BRAUNWALD, M.D., F.A.C.P.
- Requests for reprints should be addressed to Stephen E. Epstein, M.D., Cardiology Branch, National Heart Institute, Bldg. 10, Room 7B-15, Bethesda, Md. 20014.
Excerpt
Two of the more prominent manifestations of impaired cardiac function are an inability to augment the cardiac output appropriately in response to increased metabolic demands, and a diminished ability to excrete sodium, with resultant fluid accumulation and edema. Since it has recently been observed that the cardiac response to maximal and submaximal levels of exercise in both normal subjects and patients with various forms of heart disease is reduced by blockade of the beta adrenergic receptors (1), it became of interest to determine if this impairment of hemodynamic performance is associated with changes in the patterns of sodium excretion. A
This 100-word excerpt has been provided in the absence of an abstract.
Acknowledgment
The authors gratefully acknowledge the cooperation of Dr. Richard L. Kahler during the initial phases of the study.
Summario in Interlingua
Le effecto de blocage del receptores β-adrenergic con propranolol super le configuration del excretion urinari de natrium esseva studiate in 6 subjectos normal e 10 patientes con disordines cardiac. Le blocage afficeva le configuration del excretion de natrium in omne le subjectos. Iste effecto poteva esser dividite in tres grados de severitate. Le plus leve grado de alteration, observate in subjectos normal e in patientes con reducite reserva cardio-vascular, consisteva de un modification del configuration diurne del excretion de natrium non resultante in ulle alteration del excretion total in 24 horas. Un grado intermedie de affection, observate in certe patientes con morbo cardiac sed non in subjectos normal, esseva manifeste in un relentamento del augmento in le excretion de natrium occurrente como responsa a progressive augmentos del ingestion de natrium, ben que un balancia de natrium esseva ultimemente establite. Le grado le plus grave de alteration, observate in solmente un patiente con disfallimento cardiac, consisteva in un progressive retention de natrium resultante in un accrescente accumulation de liquido e edema. Ben que le resultatos del presente investigation suggestiona que blocage β-adrenergic non causa un grave retention de natrium in le majoritate del patientes cardiac, le facto es sublineate que le inhibition del activitate de nervos sympathic cardiac pote occasionalmente precipitar un periculose decompensation cardiac non associate con previe retention de natrium e ganio de peso.
Article and Author Information
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From the Cardiology Branch, National Heart Institute, National Institutes of Health, Bethesda, Md.
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- Received February 3, 1966.
- Accepted February 28, 1966.
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