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Correlaciones morfológicas y electrofisiológicas de la respuesta nodal atrioventricular al aumento de la actividad
S Imaizumi1, T Mazgalev, L S Dreifus
1Department of Medicine, Lankenau Hospital, Philadelphia, PA 19151.
Circulation
|September 1, 1990
Resumen
La estimulación vagal ralentiza el ritmo cardíaco al actuar sobre células específicas en el nodo atrioventricular (AV). Este efecto se concentra en la región nodal media, influyendo en la conducción cardíaca.
Área de la Ciencia:
- Fisiología cardiovascular fisiología cardiovascular.
- Función del sistema nervioso autónomo.
- Electrofisiología Cardíaca Electrofisiología cardíaca.
Sus antecedentes:
- Los mecanismos que ralentizan la conducción del impulso cardíaco a través del nodo atrioventricular (AV) son complejos, e implican factores anatómicos, una diversa electrofisiología celular y la modulación del sistema nervioso autónomo.
- Comprender la ubicación precisa y los objetivos celulares de la influencia del nervio vagal en la conducción nodal AV es crucial para comprender la regulación del ritmo cardíaco.
Objetivo del estudio:
- Para identificar el sitio específico de la desaceleración inducida vagalmente de la conducción del impulso cardíaco dentro del nodo AV.
- Para correlacionar las respuestas electrofisiológicas a la estimulación vagal con hallazgos morfológicos e histoquímicos en diferentes regiones nódales AV.
Principales métodos:
- La estimulación vagal postganglionar se aplicó a regiones distintas del nodo AV.
- Se registraron respuestas electrofisiológicas de las células nódales AV.
- El análisis morfológico y los patrones de tinción de la acetilcolinesterasa (AChE) se examinaron en el tejido nodal.
Principales resultados:
- La estimulación vagal causó hiperpolarización localizada en las células de la región N, en correlación con la tinción intensa de AChE en el nodo AV central.
- La densidad de tinción de AChE disminuyó hacia las regiones AN y His bundle, donde la estimulación vagal tuvo un efecto mínimo.
- La liberación de acetilcolina y su acción depresiva se concentraron en las células N midnodal.
Conclusiones:
- La desaceleración vagal de la conducción nodal AV está mediada principalmente por la liberación de acetilcolina en la región midnodal.
- Las células N en la región midnodal son los principales objetivos de los efectos vagales, lo que lleva a la hiperpolarización y potenciales de acción deprimidos.
- Una estrecha proximidad entre los elementos del nervio vago y las células N en la región midnodal facilita la neuromodulación enfocada de la conducción cardíaca.
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