Zusammenfassung
Background: Interleukin-6 (IL-6) is expressed in the myocardium and has been implicated in cell proliferation, negative inotropic effects and myocardial hypertrophy. To determine whether myocardial IL-6 is modified by neuro-humoral and immunoregulatory stimuli, we studied the effects of lipopolysaccharide (LPS), corticosterone (CS), isoproterenol and angiotensin II on myocardial IL-6 secretion in ...
Zusammenfassung
Background: Interleukin-6 (IL-6) is expressed in the myocardium and has been implicated in cell proliferation, negative inotropic effects and myocardial hypertrophy. To determine whether myocardial IL-6 is modified by neuro-humoral and immunoregulatory stimuli, we studied the effects of lipopolysaccharide (LPS), corticosterone (CS), isoproterenol and angiotensin II on myocardial IL-6 secretion in superfused myocardium. Methods: Slices of rat left ventricular myocardium were superfused in 80 mul chambers for up to 5 h. LPS (1, 50, and 100 mug/ml), CS (10(-7), 10(-6), and 10(-5) M, DSMO as vehicle), isoproterenol (10(-6), 10(-7), and 10(-8) M) and angiotensin II (10(-5), 10(-7), and 10(-9) M) were added to the culture medium at hour 2. IL-6 was measured in the perfusate by ELISA. Results: Physiological corticosterone concentrations (10(-7) M) resulted in an increase in IL-6 concentration (142%) while high doses of steroid decreased IL-6 significantly (CS 10(-6) M: 88 +/- 14%, p <.05; CS 10(-5): 91 +/- 9%, p < .05) after 5 h. Left ventricular IL-6 secretion was significantly stimulated by LPS 50 mug/ml (3262 1684% vs. CTRL: 116 +/- 134%, p < .01). Isoproterenol treatment increased in IL-6 secretion compared to controls with and without CS, while angiotensin II reduced IL-6 concentration only in combination with CS. Conclusion: Myocardial IL-6 secretion is modulated by physiological concentrations of corticosterone or angiotensin II and can be induced by LPS or isoproterenol, indicating a tight regulation of this cytokine. Suppression of cytokine expression within the heart might be a potential therapeutic goal in the treatment of various cardiovascular diseases. (C) 2003 Elsevier Science (USA). All rights reserved.
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