Sympathetic mechanisms in an animal model of vasovagal syncope.
He Wenbo,Wang Xiaoying,Liu Shan,Yu Xiaomei,Lu Zhibing,Ma Ruisong,Luo Da,Xie Jing,He Bo,Jiang Hong
Clinical autonomic research : official journal of the Clinical Autonomic Research Society
PURPOSE:Individuals predisposed to vasovagal syncope may have different autonomic nervous system control mechanisms from those without predisposition to vasovagal events. To test this hypothesis, we investigated different sympathetic responses in a canine model of vasovagal syncope. METHODS:Left thoracotomy was performed on 20 mongrel dogs. The heart was exposed and a bolus of veratridine (15 μg/kg), a neurotoxin which prevents the inactivation of sodium ion channels, was injected into the left atrium to induce a Bezold-Jarisch reflex-mediated vasovagal event, characterized by bradycardia, decreased inotropism, and hypotension. Electrocardiogram and blood pressure were continuously monitored. Neural activity was recorded from the left stellate ganglion. Plasma norepinephrine and acetylcholine levels were measured 30 s before and 30 s after veratridine injection. RESULTS:Veratridine resulted in rapid decreases in heart rate and blood pressure in all dogs, accompanied by increases in both norepinephrine and acetylcholine. Two types of neural activity (high-amplitude spike discharge activity and low-amplitude burst discharge activity) were recorded from the left stellate ganglion. Veratridine induced high-frequency spike discharge activity in some dogs (Group A), whereas spike discharge activity was scarce and relatively unresponsive to veratridine in the remaining dogs (Group B). Dogs in Group A had higher plasma norepinephrine levels (111.63 ± 15.1 vs. 48.11 ± 33.81 ng/l, p = 0.002) and less intense drops in heart rate (- 37 ± 24 vs. - 84 ± 28 bpm, p = 0.001) and blood pressure (systolic blood pressure, - 18 ± 15 vs. - 37 ± 13 mmHg, p = 0.009; diastolic blood pressure, - 26 ± 13 vs. - 45 ± 13 mmHg, p = 0.005) compared to dogs in Group B. Similarly, heart rate post-veratridine was higher (102 ± 23 vs. 69 ± 22 bpm, p = 0.004), the veratridine-induced longest RR interval was shorter (0.7 [0.5-0.8] vs. 1.2 [1.1-3.5] s, p < 0.001) and the diastolic and mean arterial pressures post-veratridine were higher (all p < 0.05) in dogs in Group A compared to those in Group B. CONCLUSIONS:Distinct sympathetic activation as represented by left stellate ganglion high-frequency spike discharge activity protected against bradycardia and hypotension in a canine model of vasovagal syncope. Our findings may have therapeutic implications.
Sympathoinhibition to Bezold-Jarisch reflex is attenuated in protein malnourished rats.
Bezerra Vanessa Moraes,Xavier Carlos Henrique,Fernandes Luciano Gonçalves,Cardoso Leonardo Máximo,Fontes Marco Antônio Peliky,Chianca Deoclécio Alves
Malnutrition affects cardiovascular reflexes, including chemoreflex and baroreflex. In this study we assessed the hypothesis that malnourishment changes the responses in mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) evoked from Bezold-Jarisch reflex (BJR). Fischer rats were fed diets containing either (6% malnourished or 14% control) protein for 35 days after weaning. There were no differences in baseline MAP (102 ± 4 vs. 95 ± 3 mmHg) whereas higher baseline HR (478 ± 18 vs. 360 ± 11 bpm; P<0.05,) and reduced sympathoinhibition (ΔRSNA=-54 ± 9 vs. -84 ± 7%; P=0.0208) to BJR activation were found in malnourished rats. We conclude that malnutrition affects the sympathetic control of BJR.