Efectos electrofisiológicos miocárdicos intrínsecos producidos por la inhibición del sistema de intercambio sodio-protón, en condiciones de normoxia, y tras la isquemia miocárdica regional. Estudio experimental.

RESUMEN Hemos investigado: 1) los efectos protectores del intercambiador sodio-protón (NHE), con el 5-(N-etil-N-isopropil) amiloride (EIPA), a concentración 0.4 M, sobre la inducibilidad de la fibrilación ventricular (FV), y sobre la refractariedad miocárdica ventricular, tras la oclusión arterial coronaria; 2) los efectos electrofisiológicos intrínsecos producidos por la inhibición del NHE, administrando EIPA 0.4 y 1 M, en condiciones de normal oxigenación, sobre el automatismo sinusal, la conducción sinoauricular y auriculoventricular (AV), y sobre la refractariedad auricular, ventricular, y del sistema de conducción AV; y 3) los efectos electrofisiológicos miocárdicos intrínsecos producidos por la inhibición del NHE, con EIPA 0.4 y 1 M, sobre la frecuencia dominante (FD) de la FV inducida, en condiciones de normoxia, como característica electrofisiológica estrechamente relacionada con la refractariedad ventricular. Todos los experimentos se realizaron en corazón aislado y perfundido de conejo (preparación tipo Langendorff). Para conseguir el primer objetivo aplicamos el test del extraestímulo (TEE) ventricular con uno, dos, y tres extraestímulos, para tratar de inducir la FV. La aplicación del primer extraestímulo sirvió además para establecer el periodo refractario objeto de investigación. Las determinaciones se realizaron previamente y tras la oclusión arterial coronaria circunfleja, en dos grupos de experimentos: control y tratados con EIPA 0.4 M. Para cumplimentar el segundo objetivo analizamos: a) periodos refractarios efectivo y funcional auricular y del sistema de conducción AV mediante el TEE auricular, periodos refractarios efectivo y funcional ventricular mediante el TEE ventricular; b) automatismo sinusal mediante la determinación de la longitud del ciclo sinusal y del tiempo de recuperación del nodo sinusal; y c) tiempo de conducción sinoauricular con el test de Narula, conducción AV y conducción ventriculoauricular retrógrada, mediante la medición de la longitud del ciclo de Wenckebach y la longitud del ciclo de Wenckebach retrógrado respectivamente. Finalmente, para acometer el tercer objetivo analizamos, por el método de Welch, la FD media, máxima y mínima de la FV inducida por estimulación a frecuencias crecientes. Los parámetros citados se estudiaron en situación control e inhibiendo el NHE, con EIPA. Utilizamos dos concentraciones de dicho inhibidor: 0.4 y 1 M; la primera se halla en el rango de la IC50 para el NHE y la segunda es la concentración más comúnmente usada en los estudios de protección miocárdica. La inhibición del NHE con EIPA 0.4 M protegió al miocardio isquémico, al dificultar la inducibilidad de la FV. Este efecto protector, probablemente está relacionado, al menos en parte, con el mantenimiento de la refractariedad ventricular en el miocardio isquémico, lo cual ha sido también observado en el presente trabajo. Excepto para el caso del periodo refractario efectivo del sistema de conducción AV, que aumentó ligeramente con EIPA 1 M, la inhibición del NHE con EIPA 0.4 y 1 M en condiciones de normal oxigenación, no modificó la refractariedad intrínseca ventricular, auricular, ni del sistema de conducción AV, así como tampoco la FD de la FV inducida, mientras que deprimió ligeramente el cronotropismo sinusal y la conducción AV, si bien estos últimos podrían ser efectos secundarios, relacionados con la capacidad depresora del automatismo sinusal y la conducción AV que ejerce el amiloride, precursor del EIPA. El hecho de que la inhibición del NHE, manifestara efectos electrofisiológicos antiarrítmicos intrínsecos sobre el miocardio isquémico, impidiendo la caída de la refractariedad, y no ejerciera ninguna modificación electrofisiológica, en condiciones de normal oxigenación, sobre la refractariedad y la FD de la FV, propiedades ligadas a la aparición de arritmias por reentrada, coincide con lo relatado por diversos investigadores acerca del escaso, sino nulo, papel del NHE en situación fisiológica y su importancia en circunstancias fisiopatológicas como la isquemia. __________________________________________________________________________________________________We have investigated the protective effects of the sodium-proton exchanger (NHE) inhibition using 5-(N-ethyl-N-isopropyl) amiloride (EIPA) 0.4 M, on the incidence of induced ventricular fibrillation (VF), and on intrinsic ventricular refractoriness, after circumflex coronary artery occlusion. Experiments were performed on isolated rabbit heart. To induce VF extrastimulus test with one, two and three extrastimuli, was used; the first extrastimulus application also served to determine refractory periods. Parameters were determined previously and after coronary occlusion, in both control and EIPA 0.4 M treated groups. In order to investigate whether the NHE inhibition produces some myocardial intrinsic electrophysiological effect, we have also investigated using EIPA, 0.4 and 1 M, in normoxic condition: a) the sinus cycle length and sinus node recovery time, as an automatism index; b) the sinoatrial conduction (Narulas test), and atrioventricular (AV) and ventricleatrial conduction, by anterograde and retrograde Wenckebach cycle length determination respectively; c) atrial, ventricular, and AV conduction system, effective and functional refractory periods using the extrastimulus test; and d) mean, minimum and maximum dominant frequency (DF) of VF by the Welchs method, which are properties closely related with ventricular refractoriness. NHE inhibition with 0.4 M protected the ischemic myocardium, decreasing VF inducibility, at least in part, by the maintenance of ischemic myocardium refractoriness, observed in this study. No modification on refractoriness was observed, in normoxic conditions, except an AV conduction system effective refractory period increase, with EIPA 1 M. The DF of VF was either not modified. EIPA 0.4 and 1 M also slightly depressed sinus chronotropism and AV conduction

Development and Long-Term Follow-Up of an Experimental Model of Myocardial Infarction in Rabbits

[EN] A chronic model of acute myocardial infarction was developed to study the mechanisms involved in adverse postinfarction ventricular remodeling. In an acute myocardial infarction (AMI), the left circumflex coronary artery of New Zealand White rabbits (n = 9) was occluded by ligature for 1 h, followed by reperfusion. A specific care protocol was applied before, during, and after the intervention, and the results were compared with those of a sham operated group (n = 7). After 5 weeks, programmed stimulation and high-resolution mapping were performed on isolated and perfused hearts using the Langendorff technique. The infarct size determined by 2,3,5-triphenyltetrazolium chloride inside of the area at risk (thioflavin-S) was then determined. The area at risk was similar in both groups (54.33% (experimental infarct group) vs. 58.59% (sham group), ns). The infarct size was 73.16% as a percentage of the risk area. The experimental infarct group had a higher inducibility of ventricular arrhythmias (100% vs. 43% in the sham group, p = 0.009). A reproducible chronic experimental model of myocardial infarction is presented in which the extent and characteristics of the lesions enable the study of the vulnerability to develop ventricular arrhythmias because of the remodeling process that occurs during cardiac tissue repair.This research was funded by Generalitat Valenciana (PROMETEO/2018/078), Instituto de Salud Carlos III (CB16/11/00486; PI15/01408; PIE15/0001 3and PI18/01620) to F.J.C.Genovés, P.; Arias-Mutis, ÓJ.; Parra, G.; Such-Miquel, L.; Zarzoso, M.; Del Canto, I.; Soler, C.... (2020). Development and Long-Term Follow-Up of an Experimental Model of Myocardial Infarction in Rabbits. Animals. 10(9). https://doi.org/10.3390/ani1009157610

The training-induced changes on automatism, conduction and myocardial refractoriness are not mediated by parasympathetic postganglionic neurons activity

The purpose of this study is to test the role that parasympathetic postganglionic neurons could play on the adaptive electrophysiological changes produced by physical training on intrinsic myocardial automatism, conduction and refractoriness. Trained rabbits were submitted to aphysical training protocol on treadmill during 6 weeks. The electrophysiological study was performed in an isolated heart preparation. The investigated myocardial properties were: (a) sinus automatism, (b) atrioventricular and ventriculoatrial conduction, (c) atrial, conduction system and ventricular refractoriness. The parameters to study the refractoriness were obtained by means of extrastimulus test at four diVerent pacing cycle lengths (10% shorter than spontaneous sinus cycle length, 250, 200 and 150 ms) and (d) mean dominant frequency (DF) of the induced ventricular Wbrillation (VF), using a spectral method. The electrophysiological protocol was performed before and during continuous atropine administration (1 ¿M), in order to block cholinergic receptors. Cholinergic receptor blockade did not modify either the increase in sinus cycle length, atrioventricular conduction and refractoriness (left ventricular and atrioventricular conduction system functional refractory periods) or the decrease of DF of VF. These Wndings reveal that the myocardial electrophysiological modiWcations produced by physical training are not mediated by intrinsic cardiac parasympathetic activity.The authors thank Carmen Rams, Ana Diaz, Pilar Navarro and Cesar Avellaneda for their excellent technical assistance. This work has been supported by grants from the Spanish Ministry of Education and Science (DEP2007-73234-C03-01) and Generalitat Valenciana (PROMETEO 2010/093). M Zarzoso was supported by a research scholarship from Generalitat Valenciana (BFPI/2008/003).Zarzoso Muñoz, M.; Such Miquel, L.; Parra Giraldo, G.; Brines Ferrando, L.; Such, L.; Chorro, F.; Guerrero, J.... (2012). The training-induced changes on automatism, conduction and myocardial refractoriness are not mediated by parasympathetic postganglionic neurons activity. European Journal of Applied Physiology. 112(6):2185-2193. https://doi.org/10.1007/s00421-011-2189-4S218521931126Armour JA, Hopkins DA (1990a) Activity of in vivo canine ventricular neurons. Am J Physiol Heart Circ Physiol 258:H326–H336. doi: 10.1152/ajpregu.00183.2004Armour JA, Hopkins DA (1990b) Activity of canine in situ left atrial ganglion neurons. Am J Physiol Heart Circ Physiol 259:H1207–H1215Armour JA (2004) Cardiac neuronal hierarchy in health and disease. Am J Physiol Regul Integr Comp Physiol 287:R262–R271Armour JA, Murphy DA, Yuan BX, Macdonald S, Hopkins DA (1997) Gross and microscopic anatomy of the human intrinsic cardiac nervous system. Anat Rec 247:289–298Bedford TG, Tipton CM (1987) Exercise training and the arterial baroreflex. J Appl Physiol 63:1926–1932Bonaduce D, Petretta M, Cavallaro V, Apicella C, Ianniciello A, Romano M, Breglio R, Marciano F (1998) Intensive training and cardiac autonomic control in high level athletes. Med Sci Sports Exerc 30:691–696Brack KE, Coote JH, Ng GA (2011) Vagus nerve stimulation protects against ventricular fibrillation independent of muscarinic receptor activation. Cardiovasc Res 91:437–446. doi: 10.1093/cvr/cvr105Brorson L, Conradson TB, Olsson B, Varnauskas E (1976) Right atrial monophasic action potential and effective refractory periods in relation to physical training and maximal heart rate. 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Circulation 115:3095–3102. doi: 10.1161/CIRCULATIONAHA.106.677989Gaustad SE, Rolim N, Wisløff U (2010) A valid and reproducible protocol for testing maximal oxygen uptake in rabbits. Eur J Cardiovasc Prev Rehabil 17:83–88. doi: 10.1097/HJR.0b013e32833090c4Gómez-Cabrera MC, Borrás C, Pallardó FV, Sastre J, Ji LL, Viña J (2005) Decreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise in rats. J Physiol 567:113–120. doi: 10.1113/jphysiol.2004.080564Gray AL, Johnson TA, Ardell JL, Massari VJ (2004) Parasympathetic control of the heart II. A novel interganglionic intrinsic cardiac circuit mediates neural control of heart rate. J Appl Physiol 96:2273–2278. doi: 10.1152/japplphysiolHamilton KL, Powers SK, Sugiura T, Kim S, Lennon S, Tumer N, Mehta JL (2001) Short-term exercise training can improve myocardial tolerance to I/R without elevation in heat shock proteins. Am J Physiol Heart Circ Physiol 281:1346–1352Inoue H, Zipes DP (1987) Changes in atrial and ventricular refractoriness and atrioventricular nodal conduction produced by combinations of vagal and sympathetic stimulation that result in a constant spontaneous sinus cycle length. Circ Res 60:942–951Jew KN, Olsson MC, Mokelke EA, Palmer BM, Moore RL (2001) Endurance training alters outward K+ current characteristics in rat cardiocytes. J Appl Physiol 90:1327–1333Johnson TA, Gray AL, Lauenstein JM, Newton SS, Massari VJ (2004) Parasympathetic control of the heart I. An interventriculo-septal ganglion is the major source of the vagal intracardiac innervation of the ventricles. J Appl Physiol 96:2265–2272. doi: 10.1152/japplphysiol.00620.2003Katona PG, McLean M, Dighton DH, Guz A (1982) Sympathetic and parasympathetic cardiac control in athletes and nonathletes at rest. J Appl Physiol 52:1652–1657Lewis SF, Nylander E, Gad P, Areskog N (1980) Non-autonomic component in bradycardia of endurance trained men at rest and during exercise. Acta Physiol Scand 109:297–305Litovsky SH, Antzelevitch C (1990) Differences in the electrophysiological response of canine ventricular subendocardium and subepicardium to acetylcholine and isoproterenol. A direct effect of acetylcholine in ventricular myocardium. Circ Res 67:615–627Löffelholz K (1981) Release of acetylcholine in the isolated heart. Am J Physiol 240(4):H431–H440Lopatin AN, Nichols CG (2001) Inward rectifiers in the heart: an update on I(K1). J Mol Cell Cardiol 33:625–638. doi: 10.1006/jmcc.2001.1344Mace LC, Palmer BM, Brown DA, Jew KN, Lynch JM, Glunt JM, Parsons TA, Cheung JY, Moore RL (2003) Influence of age and run training on cardiac Na+/Ca2+ exchange. 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Análisis de regularidad en fibrilación ventricular: aplicación a registros de mapeado cardíaco

Las técnicas utilizadas en el análisis de la señal de fibrilación ventricular (FV), obtenida mediante sistemas de mapeado utilizando matrices de electrodos, extraen información del proceso a partir de parámetros calculados principalmente en el dominio del tiempo o de la frecuencia. El presente trabajo plantea la aplicación del índice de regularidad (IR), propuesto inicialmente para caracterizar la fibrilación auricular humana, a la señal de FV en un modelo experimental de corazón animal. Los resultados obtenidos muestran que el IR permite extraer información de los mapas de FV no disponible de forma directa cuando se estudian mediante los métodos clásicos en el tiempo o la frecuencia, cuantificando el grado de modificación en la morfología de las ondas de activación durante la FV

Effect of chronic exercise on myocardial electrophysiological heterogeneity and stability. Role of intrinsic cholinergic neurons: A study in the isolated rabbit heart

[EN] A study has been made of the effect of chronic exercise on myocardial electrophysiological heterogeneity and stability, as well as of the role of cholinergic neurons in these changes. Determinations in hearts from untrained and trained rabbits on a treadmill were performed. The hearts were isolated and perfused. A pacing electrode and a recording multielectrode were located in the left ventricle. The parameters determined during induced VF, before and after atropine (1 mu M), were: fibrillatory cycle length (VV), ventricular functional refractory period (FRPVF), normalized energy (NE) of the fibrillatory signal and its coefficient of variation (CV), and electrical ventricular activation complexity, as an approach to myocardial heterogeneity and stability. The VV interval was longer in the trained group than in the control group both prior to atropine (78 +/- 10 vs. 68 +/- 10 ms) and after atropine (76 +/- 8 vs. 67 +/- 10 ms). Likewise, FRPVF was longer in the trained group than in the control group both prior to and after atropine (53 +/- 8 vs. 42 +/- 7 ms and 50 +/- 6 vs. 40 +/- 6 ms, respectively), and atropine did not modify FRPVF. The CV of FRPVF was lower in the trained group than in the control group prior to atropine (12.5 +/- 1.5% vs. 15.1 +/- 3.8%) and, decreased after atropine (15.1 +/- 3.8% vs. 12.2 +/- 2.4%) in the control group. The trained group showed higher NE values before (0.40 +/- 0.04 vs. 0.36 +/- 0.05) and after atropine (0.37 +/- 0.04 vs. 0.34 +/- 0.06; p = 0.08). Training decreased the CV of NE both before (23.3 +/- 2% vs. 25.2 +/- 4%; p = 0.08) and after parasympathetic blockade (22.6 +/- 1% vs. 26.1 +/- 5%). Cholinergic blockade did not modify these parameters within the control and trained groups. Activation complexity was lower in the trained than in the control animals before atropine (34 +/- 8 vs. 41 +/- 5), and increased after atropine in the control group (41 +/- 5 vs. 48 +/- 9, respectively). Thus, training decreases the intrinsic heterogeneity of the myocardium, increases electrophysiological stability, and prevents some modifications due to muscarinic block.This research was supported by the Spanish Ministry of Education and Science, (DEP2007-73234-C03-01 to AMA), http://www.mecd.gob.es/portada-mecd/; and the Generalitat Valenciana (PROMETEO 2010/093 to FJC, and FPI/2008/003 to MZ), http://www.gva.es/va/inicio/presentacion; jsessionid=ydprbDQZTsCTz85W1Such-Miquel, L.; Brines-Ferrando, L.; Alberola, A.; Zarzoso Muñoz, M.; Chorro Gasco, FJ.; Guerrero-Martínez, JF.; Parra-Giraldo, G.... (2018). Effect of chronic exercise on myocardial electrophysiological heterogeneity and stability. Role of intrinsic cholinergic neurons: A study in the isolated rabbit heart. 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(2011). The training-induced changes on automatism, conduction and myocardial refractoriness are not mediated by parasympathetic postganglionic neurons activity. European Journal of Applied Physiology, 112(6), 2185-2193. doi:10.1007/s00421-011-2189-4Billman, G. E. (2009). Cardiac autonomic neural remodeling and susceptibility to sudden cardiac death: effect of endurance exercise training. American Journal of Physiology-Heart and Circulatory Physiology, 297(4), H1171-H1193. doi:10.1152/ajpheart.00534.2009HAN, J., & MOE, G. K. (1964). Nonuniform Recovery of Excitability in Ventricular Muscle. Circulation Research, 14(1), 44-60. doi:10.1161/01.res.14.1.44Beaumont, E., Salavatian, S., Southerland, E. M., Vinet, A., Jacquemet, V., Armour, J. A., & Ardell, J. L. (2013). Network interactions within the canine intrinsic cardiac nervous system: implications for reflex control of regional cardiac function. The Journal of Physiology, 591(18), 4515-4533. doi:10.1113/jphysiol.2013.259382Armour, J. 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Application of machine learning techniques to analyse the effects of physical exercise in ventricular fibrillation

This work presents the application of machine learning techniques to analyze the influence of physical exercise in the heart's physiological properties, during ventricular fibrillation. With that purpose, different kinds of classifiers (linear and neural models) were used to classify between trained and sedentary rabbit hearts. These classifiers were used to perform knowledge extraction through a wrapper feature selection algorithm. The obtained results showed the higher performance of the neural models compared to the linear classifier (higher performance measures and higher dimensionality reduction). The most relevant features to describe the benefits of physical exercise are those related to myocardial heterogeneity, mean activation rate and activation complexity

Modifications on regularity and spectrum of ventricular fibrillation signal induced by physical training

The objective of this work is to study the modifications on cardiac response during ventricular fibrillation (VF) induced by physical training. The analysis was performed in the frequency domain of VF, and the regularity of the signal was also considered. Two sets of records were acquired: control (G1: without physical training, N=10), and trained (G2, N=9). Cardiac registers were obtained using a 240-electrodes matrix located on left ventricle of isolated rabbit heart. A Langendorff system was used to maintain the heart perfusion. VF was induced by increased frequencies. To analyze the time course of VF, records were processed in 4-second segments. For every segment and channel, Welch periodogram with Hanning window, two non-overlapped sections and zero padding, was computed. Parameters considered in frequency domain are: dominant frequency (DF) and normalized energy (NE: spectral energy in the window DF±1Hz, normalized by spectral energy in 5-35Hz band). For every segment and channel, a regularity analysis of VF was performed, obtaining the regularity index (RI), which is a measure of similarity among local activation waves present in every channel. Mean values for the parameters (DF, NE and RI) of the whole set of electrodes were computed for every segment. Obtained results show that DF is lower for trained rabbits (G1: 18.234±1, 241Hz; G2: 14.370±0, 866Hz; p<0.001). NE is greater for this group (G1: 0.140±0.006; G2: 0.263±0.017; p<0.001), suggesting a greater spectral concentration around DF. Finally, a greater regularity has been observed in the fibrillation signal for trained group (IR, G1: 0.756±0.026; G2: 0.834±0.014; p<0.001). As a summary, the results suggest that both spectral characteristics and regularity of VF signal are clearly different for G1 and G2 groups. The trained group (G2) shows greater regularity, lower DF and spectral dispersion. These factors should be interpreted as a more stable cardiac response to V

Analysis of spatial and temporal evolution of regularity maps during ventricular fibrillation

The analysis of cardiac mapping allows investigating the structure of ventricular fibrillation (VF). This work analyzes regions of interest (ROI) on cardiac maps obtained from the regularity analysis of VF records, providing information about signal regularity at each time instant and its spatial distribution. Cardiac registers were obtained using a 240- electrodes matrix located on left ventricle of isolated rabbit heart. A Langendorff system was used to maintain the heart perfusion. VF was induced by increased frequencies. Two groups of records were considered: control (G1: without physical training, N=10), and trained (G2, N=9). Records were processed in consecutive 4-second segments. Regularity index (RI) was obtained for every segment and channel. RI is a measure of similarity degree among local activation waves for every channel. A map with the RI value of each channel was computed for the 82 register segments. To analyze the spatial distribution of RI, a threshold value was determined experimentally and applied to the map in order to obtain the ROI. Two parameters were calculated: ROI spatial number (ROIsn, a measure of spatial fragmentation), and ROI spatial area (ROIsa, the percentage of area map occupied by ROI). In case of the time course of ROI, two additional parameters were computed: the number of electrodes which value had changed respect to the threshold in two consecutive maps (ROIen, which is related with the change size), and the cumulative absolute differences of RI values for the electrodes which are changed (ROIed). Obtained results for spatial analysis show that the number of ROI is lower for trained rabbits (ROIsn; G1: 4.465±1.120; G2: 2.,227±0.623; p<0.001), but ROI spatial area is greater than the control group (ROIsa; G1: 76.235±5.355%; G2: 88.163±2.885%; p<0.001). Time-course analysis shows that more electrodes change between consecutive maps in the control group (ROIen, G1: 22.455±6.702; G2: 13.877±2.485; p<0.001). No significant differences were found for ROIed (G1: 18.509±6.932; G2: 18.619±4.196; n.s.). To conclude, ROI analysis on RI maps applied to trained and no trained rabbits groups shows that VF cardiac response is more irregular and spatially fragmented in no trained group. In addition, regularity maps are more stable with time in trained group

Relación entre el espectro y la regularidad en la señal de fibrilación ventricular modificada por el ejercicio físico

El presente trabajo estudia las modificaciones intrínsecas que el ejercicio físico produce en la respuesta cardíaca durante la FV. Se han calculado dos parámetros relacionados con el espectro de la señal (FD: frecuencia dominante, y EN: energía normalizada), y otro relacionado con la regularidad de las OAL (IR: índice de regularidad), Se ha realizado un análisis de correlación entre los tres parámetros para valorar su grado de complementariedad. Se consideraron dos grupos de conejos: control (G1: sin entrenamiento, N=10) y entrenados (G2, N=9). Se utilizó un electrodo matricial de 240 canales localizado en ventrículo izquierdo de corazón aislado de conejo perfundido mediante un sistema de Langendorff. La FV se indujo por estimulación a frecuencias crecientes. Los resultados muestran que el grupo entrenado presenta una mayor regularidad de la señal (IR: G1: 0,757+-0,091; G2: 0,845+-0,084; p<0.001), así como menor FD (G1: 18.23±2.96Hz; G2: 14.13+-1.73Hz; p<0.001) y dispersión espectral (EN: G1: 0,138+-0.105; G2: 0,293+-0,176; p<0.001). El análisis de las relaciones entre parámetros muestra correlaciones significativas entre los parámetros para todos los casos excepto para IR y FD en G2, por lo que estos parámetros proporcionan información complementaria, ya que analizan aspectos diferentes de la señal como la morfología de las ondas de activación y su frecuencia. La existencia de correlación entre ambas para G1 puede ser debida a otras causas, tales como las modificaciones en ambos factores inducidas por la presencia de reentradas o colisiones entre frentes de activación.. Como conclusión, los resultados obtenidos sugieren que el entrenamiento físico produce una respuesta cardíaca más estable ante FV, debida a modificaciones intrínsecas en las características electrofisiológicas cardíacas

Analysis of the influence of parasympathetic postganglionic neurons on cardiac response in ventricular fibrillation

Physical training modifies the sympathetic-vagal balance of autonomic nervous system. Previous studies have shown that such training also produces intrinsic modifications of cardiac electrophysiological properties in isolated heart during Ventricular Fibrillation (VF). Ten NZW trained rabbits were studied to test if the modifications are related to the activity of postganglionic parasympathetic neurons. Two records per subject were acquired during VF: before (G1) and after (G2) the infusion of atropine to inhibit the activity of neurons. Mapping records were obtained using a 240-channel electrode array located in the left ventricle of isolated heart (perfused by Langendorff system). VF was induced by stimulation at increasing frequencies. To analyze the time course of fibrillation, the records were processed in 4-second consecutive segments. For each channel and segment, the following parameters were computed: 1) Dominant Frequency (DF), obtained by the Welch periodogram b) Normalized Energy (NE) in a frequency band centered at the DF; c) Regularity Index (RI), which analyzes the similarity of local activation waves in every segment and channel; d) Coefficients of Variance of DF (CVDF), NE (CVNE) and RI (CVRI). For each segment, we obtained the average value of each of the parameters analyzed for all electrodes. The results are: a) DF (G1: 13.671 ± 0.509 Hz, G2: 14.783 ± 0.455 Hz), b) NE (G1: 0.398 ± 0.014; G2: 0.380 ± 0.013); c) RI (G1: 0.855 ± 0.017; G2: 0.865 ± 0.015), d) CVDF (G1: 0.109 ± 0.009; G2: 0.098 ± 0.008), e) CVNE (G1: 0.398 ± 0.014; G2: 0.380 ± 0.013 ) f) CVRI (G1: 0.084 ± 0.009; G2: 0.078 ± 0.008). None of these parameters showed significant differences between groups. Thus, the parasympathetic postganglionic neurons seem to have no effect on the cardiac response in VF due to physical training