La estimulación vagal eferente preisquémica aumenta el tamaño del infarto de miocardio en conejos / Preischemic Vagal Efferent Stimulation Increases Infarct Size in Rabbits / Preischemic Vagal Efferent Stimulation Increases Infarct Size in Rabbits

La estimulación vagal induce efectos cardioprotectores y la administración de acetilcolina mimetiza el efecto del precondicionamiento isquémico. No obstante, no existen datos concluyentes con respecto a los efectos de la estimulación vagal en el infarto de miocardio in vivo. Con el objetivo de evaluar los efectos de la estimulación vagal sobre el infarto de miocardio experimental en conejos, se provocó isquemia miocárdica regional por ligadura de una rama coronaria izquierda durante 45 min seguida de 4 horas de reperfusión (G1, n = 14). En el grupo 2 (G2, n = 9) se repitió el protocolo de G1 aplicándose, antes de la isquemia, estimulación vagal eferente derecha durante 10 min a una intensidad tal que produjo una reducción de la frecuencia cardíaca de entre el 10% y el 20%, seguida de 5 min de recuperación. En el grupo 3 (G3, n = 5) se repitió el protocolo de G2, pero se administró atropina durante la estimulación vagal. En otros grupos experimentales se repitió el protocolo de G2, pero administrando un bloqueante adrenérgico β1 de acción corta (esmolol) durante la estimulación (G4, n = 7) o uno de acción prolongada (atenolol) (G5, n = 5). La estimulación vagal preisquemia aumentó el tamaño del infarto desde el 45,2% ± 2,4% al 62,9% ± 3,1% (p < 0,05). La atropina revirtió este efecto, reduciéndolo al 44,8% ± 3,9% (p < 0,05 vs. G2). La administración de esmolol o de atenolol atenuó el incremento del tamaño del infarto al 50,1% ± 4,2% y al 50,0% ± 2,9%, respectivamente (p < 0,05). La estimulación vagal eferente preisquémica incrementa significativamente el tamaño del infarto por un mecanismo colinérgico muscarínico, efecto que es revertido por bloqueo beta-adrenérgico. La estimulación vagal, aplicada en diversas situaciones clínicas, podría causar efectos secundarios perjudiciales.

It has been shown that vagal stimulation induces cardioprotective effects and the administration of acetylcholine mimics ischemic preconditioning. However, there are no conclusive data about the effects of in vivo vagal stimulation on myocardial infarction. The objective of this study was to evaluate the effects of vagal stimulation on experimental myocardial infarction induced in rabbits subjected to 45 min of regional myocardial ischemia by ligation of a branch of the left coronary artery, followed by 4 hours of reperfusion (G1, n=14). In group 2 (G2, n=9) G1 protocol was repeated and, before inducing ischemia, right efferent vagal stimulation was performed during 10 min to an intensity enough to reduce heart rate by 10-20% followed by a recovery period of 5 min. In group 3 (G3, n=5) the G2 protocol was repeated, but atropine was administered during vagal stimulation. In other experimental groups the G2 protocol was repeated and short-acting β1 -adrenergic blocker (esmolol, G4, n=7) or long-acting beta blocker (atenolol, G5, n=5) were administered during the stimulation. Preischemic vagal stimulation increased the infarct size from 45.2%±2.4% to 62.9%±3.1% (p <0.05). Atropine reverted this effect reducing the infarct size to 44.8%±3.9% (p <0.05 vs. G2). The administration of esmolol or atenolol attenuated the increase in infarct size to 50.1%±4.2% and 50.0%±2.9%, respectively (p <0,05). Preischemic efferent vagal stimulation significantly increases the infarct size by a muscarinic cholinergic mechanism. This effect is reverted by beta adrenergic blockade. Applying vagal stimulation to different clinical scenarios might cause deleterious secondary effects.

The Effectiveness for Vagal Stimulation by Ice Water Application to Face during Controlled Respiration and Mechanism of Individual Variability of Responsiveness to Vagal Stimulation (Power Spectral Analysis of Heart Rate Variability)

BACKGROUND: The effectiveness for vagal stimulation by ice water aplication to face during metronome-controlled respiration of 15 breaths/minute was examed. The importance of basal vagal tone and sympathovagal interaction in the individual variability of responsiveness to the vagal stimulation was investigated. METHOD: Fifty three 12~13 year old healthy volunteers were included. Vagal tone and sympathovagal interaction before and after application of ice water to the face were assessed by power spectral analysis of RR interval(heart rate) variability. RESULT: Basal heart rate, high frequency power, and low to high frequency power ratio were 81+/-13(58~110 beats/min), 791+/-1061(56~4161 msec2) and 1.08+/-1.22(0.04~4.85) during controlled respiration. After ice water application twenty three children developed 5 more nodal escape beats due to severe bradycardia. Minimum heart rate, high frequency power and low to high power ratio changed to 42+/-12(19~72/min), 1890+/-1882(221~7258msec2) and 0.64+/-0.43(0.12~1.46). The increased ratio of high frequency power, maximum heart rate decrement and its percent after stimulation were 5.44+/-5.62(0.63~24.26), 39+/-14(10~81/min) and 47+/-15(16~81%) respectively. The increased ratio of high frequency power was correlated with basal logarithmic high frequency power(r=-0.60, p=0.0004). Maximum heart rate decrement was correlated with basal logarithmic high frequency power(r=-0.41, p=0.0018) and low to high frequency power ratio(r=0.27, p=0.04). CONCLUSION: Application of ice water to the face during controlled respiration produces powerful vagal stimulation and bradycardia, however, there is a wide individual variability of responsiveness to it. The absolute basal vagal tone contribute to this individual variability.

A Study of Individual Variation of Responsiveness to Vagal Stimulation in Children (Nonspectral Analysis)

BACKGROUND: It is well known that there is wide individual variation of responsiveness when parasympathetic nervous system is stimulated physiologically, pathologically, and therapeutically. But no appropriate explanation is present for that yet. So the purpose of this study is to verify individual diversity of vagal tone during resting state and after vagal stimulation and to find factor that may significantly contribute to it. METHOD: We serially measured variation of heart period(VHP : sec) which had been known to be an accurate index of cardiac parasympathetic tone during resting state(VHPb) and after vagal stimulation by ice water application to face(VHPv). And we analyzed correlation between VHPb, VHPv and ratio of VHPv to VHPb(ratio). RESULT: There was wide variation of vagal tone both in resting state (VHPb : 0.025-0.161) and after vagal stimulation (VHPv : 0.087-0.661). VHPb could be classified into 3 groups according to stem and leaf distribution(group A : VHPb could be classified into 3 groups according to stem and leaf distribution(group A : VHPb0.1). The low VHPb group A showed dramatic increase in vagal tone after vagal stimulation (ratio 2.21-20.24 mean 7.7), on the other hand high VHPb group C did not (ratio 0.80-2.55 mean 1.39). There ws also a significant negative correlation between VHPb and ratio (r=0.69, p<0.001). CONCLUSION: These results suggest that there is wide individual diversity of responsiveness to vagal stimulation and magnitude of vagal tone in resting state is an important factor to determine the responsiveness to vagal stimulation.