Key result
Serum immunoglobulins from patients with myocarditis and dilated cardiomyopathy caused in vitro acceleration of neonatal rat heart myocytes, an effect inhibited by beta-1 adrenergic antagonists.
Why the study?
Do immunoglobulins from patients with myocarditis and dilated cardiomyopathy cause beta-adrenergic agonism in neonatal rat heart myocytes?
Do immunoglobulins from patients with myocarditis and dilated cardiomyopathy cause beta-adrenergic agonism in neonatal rat heart myocytes?
Autoantibodies in myocarditis and dilated cardiomyopathy act as beta-adrenergic agonists without causing receptor desensitization, potentially contributing to disease pathogenesis.
Autoantibody beta-agonism in rat myocytes should not change practice; leaves open relevance to human myocarditis/DCM pathogenesis.
The serum of patients with myocarditis and dilated cardiomyopathy contains immunoglobulins capable of causing in vitro acceleration of beating of neonatal rat heart myocytes. This effect is stereoselectively inhibited by (-)-propranolol and is inhibited also by the beta 1-selective adrenergic antagonists, bisoprolol and metoprolol. This effect is not reversed by washing and continues unabated for at least 24 h.
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Wallukat et al. (1991) studied myocarditis and dilated cardiomyopathy. Serum immunoglobulins from patients with myocarditis and dilated cardiomyopathy was evaluated on in vitro acceleration of beating of neonatal rat heart myocytes. Serum immunoglobulins from patients with myocarditis and dilated cardiomyopathy caused in vitro acceleration of neonatal rat heart myocytes, an effect inhibited by beta-1 adrenergic antagonists.
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