Abstract
RESUMO Objetivo: estudar a dinâmica do comportamento do esôfago humano quando afetado por doença de Chagas e propor um controlador orgânico para auxiliar no aperistaltismo do órgão. Métodos: um modelo de massa, mola e amortecedor foi proposto para modelar o deslocamento do bolo alimentar no esôfago durante a ação peristáltica. Foram utilizados parâmetros da literatura para simular o megaesôfago chagásico e o saudável. Resultados: foram analisadas as curvas de velocidade e deslocamento de ambos os modelos e identificou-se as diferenças dinâmicas entre o órgão saudável e um doente. O deslocamento de alimentos em um tipo de Chagas megaesófago II (3 centímetros de dilatação) é apenas 11,84% do deslocamento num esófago saudável. Conclusão: a doença de chagas gera uma velocidade próxima de zero e um alto amortecimento na curva de descida do alimento que devido ao peristaltismo o deslocamento que não pode retornar ao seu estado inicial, o que comprova a retenção do bolo alimentar. Com o sistema de controle orgânico proposto obteve-se uma aproximação das curvas a um comportamento dinâmico próximo do modelo do órgão saudável, minimizando a retenção do alimento.
Highlights
The movement of the bolus in the esophagus is a result of the neural stimulations and the contraction responses its muscular wall, generating peristaltic forces that are responsible for the food bolus transport to the end of the organ[1]
Chagas disease generates a velocity close to zero and a high dampering in the downwards curve of the bolus whose displacement cannot return to its initial state, due to aperistalses, which proves the food bolus retention
With the introduction of the proposed organic control system, an approximation of the curves that remained with dynamic behavior close to the model of the healthy organ was obtained, minimizing the retention of the food
Summary
The movement of the bolus in the esophagus is a result of the neural stimulations and the contraction responses its muscular wall, generating peristaltic forces that are responsible for the food bolus transport to the end of the organ[1]. The esophageal Chagas disease is characterized by inflammatory lesions in the enteric nervous system, associated with a drastic reduction in the number of active nerves. As a result of the intrinsic denervation, there is a motor incoordination, a retention of the food bolus transport, a muscular hypertrophy and, an esophageal dilatation, leading to the formation of the chagasic megaesophagus[2,3,4]. Studies on the gastrointestinal aspects of Chagas disease are important for allowing the development of a natural model to comprehend the consequences of the destruction of the enteric nervous system in humans[8]. Drugs available for the treatment merely kill extracellular parasites and the nerve damage they cause is irreversible”[9]
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