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Carvedilol increases the production of interleukin-12 and interferon-gamma and improves the survival of mice infected with the encephalomyocarditis virus.
J Am Coll Cardiol. 2003 Jan 15; 41(2):340-5.JACC

Abstract

OBJECTIVES

This study was designed to examine the effects of carvedilol in a murine model of viral myocarditis induced by encephalomyocarditis virus (EMCV) infection.

BACKGROUND

Cytokines play an important role in the pathophysiology of viral myocarditis. Catecholamines influence the production of cytokines via beta-adrenergic receptors, suggesting that beta-adrenergic blockers could modulate the production of cytokines and exert a therapeutic effect in viral myocarditis by blocking the beta-stimulating action of endogenous catecholamines. In clinical trials, the third-generation, nonselective beta-blocker carvedilol was the first among several beta-blockers to reduce mortality in heart failure. However, the effects of carvedilol in acute viral myocarditis and on cytokine production are unknown.

METHODS

This study compared the effects of carvedilol, the selective beta(1)-blocker metoprolol, and the nonselective beta-blocker propranolol in a murine model of viral myocarditis induced by EMCV.

RESULTS

Carvedilol improved the 14-day survival of the animals, attenuated myocardial lesions on day 7, and increased myocardial levels of interleukin (IL)-12 and interferon (IFN)-gamma, whereas reducing myocardial virus replication. Propranolol also attenuated myocardial lesions, but to a lesser extent, and increased IL-12 and IFN-gamma levels. Metoprolol had no effect in this model. Encephalomyocarditis virus infection increased plasma catecholamine levels.

CONCLUSIONS

These results suggest that by blocking the beta(2)-stimulating effects of catecholamines, carvedilol exerts some of its beneficial effects by increasing the production of IL-12 and IFN-gamma. Carvedilol may be effective in patients with viral myocarditis by boosting IL-12 and IFN-gamma production.

Authors+Show Affiliations

Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Japan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12535832

Citation

Nishio, Ryosuke, et al. "Carvedilol Increases the Production of Interleukin-12 and Interferon-gamma and Improves the Survival of Mice Infected With the Encephalomyocarditis Virus." Journal of the American College of Cardiology, vol. 41, no. 2, 2003, pp. 340-5.
Nishio R, Shioi T, Sasayama S, et al. Carvedilol increases the production of interleukin-12 and interferon-gamma and improves the survival of mice infected with the encephalomyocarditis virus. J Am Coll Cardiol. 2003;41(2):340-5.
Nishio, R., Shioi, T., Sasayama, S., & Matsumori, A. (2003). Carvedilol increases the production of interleukin-12 and interferon-gamma and improves the survival of mice infected with the encephalomyocarditis virus. Journal of the American College of Cardiology, 41(2), 340-5.
Nishio R, et al. Carvedilol Increases the Production of Interleukin-12 and Interferon-gamma and Improves the Survival of Mice Infected With the Encephalomyocarditis Virus. J Am Coll Cardiol. 2003 Jan 15;41(2):340-5. PubMed PMID: 12535832.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Carvedilol increases the production of interleukin-12 and interferon-gamma and improves the survival of mice infected with the encephalomyocarditis virus. AU - Nishio,Ryosuke, AU - Shioi,Tetsuo, AU - Sasayama,Shigetake, AU - Matsumori,Akira, PY - 2003/1/22/pubmed PY - 2003/3/5/medline PY - 2003/1/22/entrez SP - 340 EP - 5 JF - Journal of the American College of Cardiology JO - J Am Coll Cardiol VL - 41 IS - 2 N2 - OBJECTIVES: This study was designed to examine the effects of carvedilol in a murine model of viral myocarditis induced by encephalomyocarditis virus (EMCV) infection. BACKGROUND: Cytokines play an important role in the pathophysiology of viral myocarditis. Catecholamines influence the production of cytokines via beta-adrenergic receptors, suggesting that beta-adrenergic blockers could modulate the production of cytokines and exert a therapeutic effect in viral myocarditis by blocking the beta-stimulating action of endogenous catecholamines. In clinical trials, the third-generation, nonselective beta-blocker carvedilol was the first among several beta-blockers to reduce mortality in heart failure. However, the effects of carvedilol in acute viral myocarditis and on cytokine production are unknown. METHODS: This study compared the effects of carvedilol, the selective beta(1)-blocker metoprolol, and the nonselective beta-blocker propranolol in a murine model of viral myocarditis induced by EMCV. RESULTS: Carvedilol improved the 14-day survival of the animals, attenuated myocardial lesions on day 7, and increased myocardial levels of interleukin (IL)-12 and interferon (IFN)-gamma, whereas reducing myocardial virus replication. Propranolol also attenuated myocardial lesions, but to a lesser extent, and increased IL-12 and IFN-gamma levels. Metoprolol had no effect in this model. Encephalomyocarditis virus infection increased plasma catecholamine levels. CONCLUSIONS: These results suggest that by blocking the beta(2)-stimulating effects of catecholamines, carvedilol exerts some of its beneficial effects by increasing the production of IL-12 and IFN-gamma. Carvedilol may be effective in patients with viral myocarditis by boosting IL-12 and IFN-gamma production. SN - 0735-1097 UR - https://www.unboundmedicine.com/medline/citation/12535832/Carvedilol_increases_the_production_of_interleukin_12_and_interferon_gamma_and_improves_the_survival_of_mice_infected_with_the_encephalomyocarditis_virus_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0735109702027110 DB - PRIME DP - Unbound Medicine ER -