title: Sera from chronic chagasic patients with complex cardiac arrhythmias depress electrogenesis and conduction in isolated rabbit hearts.
abstract: BACKGROUND
  Immune dysfunction has long been proposed as a mechanism for the etiopathogenesis of the chronic phase of Chagas' disease. Antibodies of chagasic patients have been shown to interfere with electric and mechanical activity of embryonic myocardial cells in culture. Here, we demonstrate that antibodies derived from a group of chronic chagasic patients are able to induce disturbances in the electrogenesis and conduction in isolated adult rabbit hearts.
  
  
  RESULTS
  Sera from chronic chagasic patients with complex cardiac arrhythmias (ChA+) decreased heart rate (from 131+/-26 to 98+/-37 bpm [mean+/-SD]; n=6; P<.05) in isolated rabbit hearts when perfused at a dilution of 1:100 (vol:vol) by the Langendorff method. Sera from another experimental group of four chronic chagasic patients without complex arrhythmias (ChA-) and two control groups composed of five Wolff-Parkinson-White (WPW) syndrome patients and five orthopedic surgery patients did not affect heart rate when tested under similar conditions. In addition, sera from five of six ChA+ patients and from one WPW patient induced AV conduction blockade. Effects of the sera from ChA+ patients are due to their IgG fractions. Both serum and IgG effects are blocked by atropine (10 micromol/L).
  
  
  CONCLUSIONS
  Antibodies of ChA+ patients decrease heart rate and induce AV conduction block in isolated adult rabbit hearts through activation of muscarinic receptors.
authors.affiliation: Instituto de Biofisica Carlos Chagas Filho, Centro de Ciências da Saúde, bloco G, UFRJ, Rio de Janeiro, Brasil.
authors.forename: S F
authors.initials: SF
authors.lastname: de Oliveira
authors.forename: R C
authors.initials: RC
authors.lastname: Pedrosa
authors.forename: J H
authors.initials: JH
authors.lastname: Nascimento
authors.forename: A C
authors.initials: AC
authors.lastname: Campos de Carvalho
authors.forename: M O
authors.initials: MO
authors.lastname: Masuda
mesh_terms: D000328:Adult; D000818:Animals; D000913:Antibodies, Protozoan / Q000276:immunology*; D001283:Atrioventricular Node / Q000187:drug effects / Q000276:immunology / Q000503:physiopathology; D001285:Atropine / Q000494:pharmacology; D002311:Cardiomyopathy, Dilated / Q000276:immunology / Q000469:parasitology / Q000503:physiopathology*; D002598:Chagas Cardiomyopathy / Q000276:immunology* / Q000503:physiopathology; D014355:Chagas Disease / Q000097:blood / Q000276:immunology*; D002908:Chronic Disease; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006327:Heart Block / Q000276:immunology / Q000469:parasitology / Q000503:physiopathology*; D006339:Heart Rate; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D018727:Muscarinic Antagonists / Q000494:pharmacology; D011817:Rabbits; D014927:Wolff-Parkinson-White Syndrome / Q000276:immunology / Q000469:parasitology / Q000503:physiopathology*
chemical_list: D000913:Antibodies, Protozoan; D007074:Immunoglobulin G; D018727:Muscarinic Antagonists; D001285:Atropine