Borda E S, Sterin-Borda L
Department of Pharmacology, School of Dentistry and Medicine, University of Buenos Aires, CEFYBO-CONICET, Argentina.
Int J Cardiol. 1996 May;54(2):149-56. doi: 10.1016/0167-5273(96)02592-2.
Evidence accumulated over the last decade gives adequate proof for the existence of circulating antibodies in Chagas' disease which bind to beta adrenergic and muscarinic cholinergic receptors of myocardium. The interaction of antibodies with cardiac neurotransmitter receptors behaving as an agonist, triggers intracellular signal transductions in the cells that alter the physiological behaviour of the heart. These events convert the normal to pathologically active cells. The interaction of antibodies against heart beta adrenergic and cholinergic receptors triggers physiologic, morphologic, enzymatic and molecular alterations, leading to cardiac damage. The analysis of the prevalence and distribution of these antibodies shows a strong association with seropositive asymptomatic patients with autonomic dysfunction in comparison with those asymptomatic without alteration of the heart autonomic disorders. The presence of these antibodies may thus partially explain the cardiomyoneuropathy of Chagas' disease, in which the sympathetic and parasympathetic systems are affected. The deposit of autoantibodies on the myocardial neurotransmitter receptors, behaving like an agonist, induced desensitization and/or down regulation of the receptors. This in turn, could lead to a progressive blockade of myocardium neurotransmitter receptors, with sympathetic and parasympathetic dennervation, a phenomenon that has been described in the course of Chagas cardioneuropathy.
过去十年积累的证据充分证明,恰加斯病(南美洲锥虫病)存在循环抗体,这些抗体可与心肌的β-肾上腺素能和毒蕈碱胆碱能受体结合。抗体与充当激动剂的心脏神经递质受体相互作用,会触发细胞内信号转导,改变心脏的生理行为。这些事件将正常细胞转变为病理活性细胞。抗心脏β-肾上腺素能和胆碱能受体抗体的相互作用会引发生理、形态、酶学和分子改变,导致心脏损伤。对这些抗体的患病率和分布分析表明,与无心脏自主神经功能紊乱改变的无症状患者相比,血清反应阳性且伴有自主神经功能障碍的无症状患者与之有很强的关联性。因此,这些抗体的存在可能部分解释了恰加斯病的心肌神经病变,其中交感和副交感神经系统均受到影响。自身抗体像激动剂一样沉积在心肌神经递质受体上,会导致受体脱敏和/或下调。反过来,这可能导致心肌神经递质受体逐渐被阻断,出现交感和副交感神经去神经支配,这一现象在恰加斯心肌神经病变过程中已有描述。