Heart rhythm · 2019
Antiarrhythmic and proarrhythmic effects of subcutaneous nerve stimulation in ambulatory dogs.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wan Juyi, Chen Mu, Yuan Yuan, Wang Zhuo, Shen Changyu, Fishbein Michael C, Chen Zhenhui, Wong Johnson, Grant Maria B, Everett Thomas H, Chen Peng-Sheng
Аннотация
BACKGROUND: High output subcutaneous nerve stimulation (ScNS) remodels the stellate ganglia and suppresses cardiac arrhythmia.
OBJECTIVE: The purpose of this study was to test the hypothesis that long duration low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of paroxysmal atrial tachycardia (PAT) in ambulatory dogs.
METHODS: We prospectively randomized 22 dogs (11 males and 11 females) into 5 different output groups for 2 months of ScNS: 0 mA (sham) (n = 6), 0.25 mA (n = 4), 1.5 mA (n = 4), 2.5 mA (n = 4), and 3.5 mA (n = 4).
RESULTS: As compared with baseline, the changes in the durations of PAT episodes per 48 hours were significantly different among different groups (sham, -5.0 ± 9.5 seconds; 0.25 mA, 95.5 ± 71.0 seconds; 1.5 mA, -99.3 ± 39.6 seconds; 2.5 mA, -155.3 ± 87.8 seconds; and 3.5 mA, -76.3 ± 44.8 seconds; P < .001). The 3.5 mA group had a greater reduction in sinus heart rate than did the sham group (-29.8 ± 15.0 beats/min vs -14.5 ± 3.0 beats/min; P = .038). Immunohistochemical studies showed that the 0.25 mA group had a significantly increased while 2.5 mA and 3.5 mA stimulation had significantly reduced growth-associated protein 43 nerve densities in both atria and ventricles. The plasma norepinephrine concentrations in the 0.25 mA group was 5063.0 ± 4366.0 pg/mL, which was significantly higher than that in the other groups of dogs (739.3 ± 946.3; P = .009). There were no significant differences in the effects of simulation between males and females.
CONCLUSION: In ambulatory dogs, low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of PAT episodes while high output ScNS is antiarrhythmic.
OBJECTIVE: The purpose of this study was to test the hypothesis that long duration low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of paroxysmal atrial tachycardia (PAT) in ambulatory dogs.
METHODS: We prospectively randomized 22 dogs (11 males and 11 females) into 5 different output groups for 2 months of ScNS: 0 mA (sham) (n = 6), 0.25 mA (n = 4), 1.5 mA (n = 4), 2.5 mA (n = 4), and 3.5 mA (n = 4).
RESULTS: As compared with baseline, the changes in the durations of PAT episodes per 48 hours were significantly different among different groups (sham, -5.0 ± 9.5 seconds; 0.25 mA, 95.5 ± 71.0 seconds; 1.5 mA, -99.3 ± 39.6 seconds; 2.5 mA, -155.3 ± 87.8 seconds; and 3.5 mA, -76.3 ± 44.8 seconds; P < .001). The 3.5 mA group had a greater reduction in sinus heart rate than did the sham group (-29.8 ± 15.0 beats/min vs -14.5 ± 3.0 beats/min; P = .038). Immunohistochemical studies showed that the 0.25 mA group had a significantly increased while 2.5 mA and 3.5 mA stimulation had significantly reduced growth-associated protein 43 nerve densities in both atria and ventricles. The plasma norepinephrine concentrations in the 0.25 mA group was 5063.0 ± 4366.0 pg/mL, which was significantly higher than that in the other groups of dogs (739.3 ± 946.3; P = .009). There were no significant differences in the effects of simulation between males and females.
CONCLUSION: In ambulatory dogs, low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of PAT episodes while high output ScNS is antiarrhythmic.