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[Changes in lymphocyte beta-receptor density in patients with heart failure before and after metoprolol or captopril
Insights
Beta-receptor density decreases in severe congestive heart failure (CHF). Metoprolol therapy increased beta-receptor density in CHF patients, suggesting beta-blockers are beneficial for treating certain heart conditions.
Area of Science:
- Cardiology
- Pharmacology
Context:
- Heart failure is a complex condition affecting cardiac function.
- Beta-adrenergic receptors play a crucial role in cardiovascular regulation.
- Understanding receptor density changes in heart disease is vital for therapeutic development.
Purpose:
- To investigate human lymphocyte beta-receptor density in heart diseases.
- To compare beta-receptor density and ejection fraction in congestive heart failure (CHF) before and after treatment.
- To evaluate the action and safety of beta-blockers in CHF management.
Summary:
- Beta-receptor density was significantly lower in severe CHF (degree III and IV) compared to normal controls.
- Metoprolol treatment up-regulated beta-receptor density in CHF patients, while captopril did not.
- Ejection fraction improved with both metoprolol and captopril, indicating enhanced cardiac function.
Impact:
- Beta-receptor density is reduced in certain types of CHF, irrespective of etiology.
- Beta-blocker therapy, specifically metoprolol, can up-regulate beta-receptor density.
- These findings support the rational use of beta-blockers in specific CHF cases, potentially mitigating negative inotropic effects when used with conventional therapy.
Abstract:
Human lymphocyte beta-receptor density in heart diseases with various degrees of heart function of 41 cases was determined. beta-receptor density and ejection fraction in congestive heart failure (CHF) before and after conventional therapy with small dose of beta-blocker (metoprolol) or captopril were compared. The aim was to clarify the action and safety of beta-blocker in the treatment of CHF. The results revealed that there was no statistical difference between beta-receptor density in CHF with cardiac function of degree I and II (516.57 +/- 85.93 fmol/10(7) cells, mean +/- s) and in normal controls (576.56 +/- 97.18 fmol/10(7) cells, P > 0.05), while beta-receptor density in CHF of degree III and IV was much lower than that in normal controls (decreased by 50%). There was no statistical difference of beta-receptor density between rheumatic heart disease and cardiomyopathy. Metoprolol up-regulated beta-receptor density from 302.40 +/- 100.91 to 459.60 +/- 174.34 fmol/10(7) cells (P < 0.05), but no change was observed after treatment by captopril. Ejection fraction was increased in both groups (P < 0.01). The results revealed that beta-receptor density was decreased in certain kinds of CHF but no relationship was observed between CHF of different etiology. beta-receptor density was up-regulated by beta-blocker, thus it indicates that it is rational to use beta-blocker for the treatment of certain kinds of CHF. And the use of small dose of beta-blocker with conventional therapy of heart failure might reduce the negative inotropic action of the former.