Introduction: The function of the Intrinsic Cardiac Nervous System is largely unknown, as is its role in heart disease. In the digestive system, a topic application of Benzalkonium chloride leads to intrinsic denervation of the viscera. Thus, our aim was to obtain an experimental model of cardiac intrinsic denervation by the application of Benzalkonium chloride on the heart. Method: Thirty male Wistar rats received intrapericardial injections of 0.3% Benzalkonium chloride (BC animals) and thirty similar animals received saline (C animals). After 15 days the animals were divided in three groups, with 10 CBtreated and 10 saline-treated animals in each. Group I was submitted to radiological and morphologic studies. The cardiac shadow area (CSA) and cardiothoracic index were calculated in roentgenograms with a semi-automatic image analysis system (MINI-MOP). The day after the animals were weighed and sacrificed with heart, liver and lung collected for histopathologic analysis. The animals of Group II were submitted to a hemodynamic study. Measurements of blood pressure, heart rate and cardiac output were performed using the Cardiomax II thermodilution system and a Thermistor sensor. With the animals of the Group III, the integrity of the extrinsic parasympathetic cardiac innervation was examined by measuring heart rate response to electrical stimulation of the right vagus. Electrical activity was assessed by ECG.Results: CB animals presented increases in cardiothoracic index, CSA, body and liver weight. In these animals the histopathologic analysis showed passive chronic congestion and reduction of the number of atrial neurons. In the hemodynamic study, total peripheral resistance and heart rate were similar in both groups, but blood pressure and cardiac index were reduced in the CB group. The vagal stimulation and ECG were similar in both groups.Conclusion: Intrinsic Cardiac Nervous System denervation caused dilated cardiopathy in rats with left and right heart failure. The etiology of some dilated cardiopathies in human is largely unknown. This unpublished experimental model should provide future studies with the objective of elucidating the relationship between neuronal injures and heart disease.