Enhancingin vivo effect of propranolol on human lymphocyte function is not due to stereospecific beta-adrenergic blockade

Mangge, Harald; Pietsch, Benjamin; Lindner, Wolfgang; Warnkroß, H; Leb, G.; Schauenstein, Konrad

doi:10.1007/bf01976221

Cited by 7 publications

(2 citation statements)

References 22 publications

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“…Blockade of adrenergic receptors, especially ␤-receptors, inhibits immunosuppression caused by catecholamines and has an immunomodulating effect (9,21,22). A few studies have demonstrated beneficial effects of ␤-blockers in viral myocarditis.…”

mentioning

confidence: 99%

Propranolol ameliorates and epinephrine exacerbates progression of acute and chronic viral myocarditis

Wang

Meissner²,

Malek³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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ameliorates and epinephrine exacerbates progression of acute and chronic viral myocarditis. Am J Physiol Heart Circ Physiol 289: H1577-H1583, 2005. First published May 27, 2005 doi:10.1152/ajpheart.00258.2005.-Recent studies point to important interactions between proinflammatory cytokines and neurohumoral mediators in heart failure. Here we investigate the influence of the ␤-adrenergic system on cytokines and neurohumoral factors and the sequelae of viral myocarditis. In an experimental model with virus-infected BALB/c mice, we studied the acute and chronic effects of epinephrine and propranolol on myocardial morphology, cytokine gene expression, and survival. BALB/c mice were inoculated with the encephalomyocarditis virus (EMCV) or sham inoculated with saline and followed for 30 days. Epinephrine increased the severity of inflammatory cell infiltration and myocardial necrosis induced by EMCV. Gene expression of TNF-␣, IL-6, and IL-10 was markedly enhanced by epinephrine in EMCV-inoculated mice. Survival rate after 30 days was reduced to 40% in epinephrine-treated EMCVinoculated mice compared with 70% in untreated EMCV-inoculated mice (P Ͻ 0.05). Treatment with the ␤-blocker propranolol significantly decreased mortality, myocardial necrosis, and infiltration of inflammatory cells in EMCV-inoculated mice. Propranolol also suppressed gene expression of TNF-␣, IL-6, and IL-10. A single dose of epinephrine 120 days after EMCV inoculation caused sudden death in 70% of infected mice; propranolol significantly reduced incidence of death to 33%. These results indicate that acute and chronic stages of viral myocarditis are modulated by the ␤-adrenergic system and its interactions with proinflammatory cytokines.

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confidence: 99%

Propranolol ameliorates and epinephrine exacerbates progression of acute and chronic viral myocarditis

Wang

Meissner²,

Malek³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

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“…In agreement with these observations, it was shown that treatment of human subjects with the b-AR antagonist propranolol increased spontaneous and PHA-induced IL-2R expression as well as IL-2 generation in circulating lymphocytes (Malec et al 1990), although the actual involvement of b-ARs in this effect of propranolol has been subsequently questioned (Mangge et al 1993). The b-AR isoprenaline inhibits the anti-CD3 mAb-induced proliferation of T cells, without synergistic effects with dexamethasone.…”

Section: Functional Responses To Ar Activationmentioning

confidence: 72%