International journal of cardiology · 2018
Ivabradine does not acutely affect open-loop baroreflex static characteristics and spares sympathetic heart rate control in rats.
СтатьяНазвание и аннотация: Перевод в очереди
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.
Yamamoto Hiromi, Kawada Toru, Shimizu Shuji, Uemura Kazunori, Inagaki Masashi, Kakehi Kazuyoshi, Iwanaga Yoshitaka, Fukuda Kanji, Miyamoto Tadayoshi, Miyazaki Shunichi, Sugimachi Masaru
Аннотация
AIMS: To assess the acute effects of intravenous ivabradine, a selective bradycardic agent, on carotid sinus baroreflex-mediated sympathetic arterial pressure (AP) and heart rate (HR) responses.
METHODS AND RESULTS: In anesthetized and vagotomized Wistar-Kyoto rats (n=6), carotid sinus baroreceptor regions were isolated. Changes in splanchnic sympathetic nerve activity (SNA), AP, and HR in response to a step-wise pressure input were examined before and after intravenous ivabradine (2mg/kg). Ivabradine did not affect the response range of SNA (91.8±6.5 vs. 93.5±9.8%) or AP (89.6±10.6 vs. 91.0±9.7mmHg). Ivabradine significantly reduced the minimum HR from 369.4±8.4 to 223.3±13.2 (P<0.001) but did not attenuate the HR response range (69.1±7.0 vs. 82.5±9.6beats/min).
CONCLUSIONS: Ivabradine does not acutely affect baroreflex-mediated sympathetic AP regulation and also spares the magnitude of the sympathetic HR response, despite significant bradycardia. The preserved sympathetic HR response, which could not be afforded by beta-blockers, may contribute to some beneficial clinical effects of ivabradine.
METHODS AND RESULTS: In anesthetized and vagotomized Wistar-Kyoto rats (n=6), carotid sinus baroreceptor regions were isolated. Changes in splanchnic sympathetic nerve activity (SNA), AP, and HR in response to a step-wise pressure input were examined before and after intravenous ivabradine (2mg/kg). Ivabradine did not affect the response range of SNA (91.8±6.5 vs. 93.5±9.8%) or AP (89.6±10.6 vs. 91.0±9.7mmHg). Ivabradine significantly reduced the minimum HR from 369.4±8.4 to 223.3±13.2 (P<0.001) but did not attenuate the HR response range (69.1±7.0 vs. 82.5±9.6beats/min).
CONCLUSIONS: Ivabradine does not acutely affect baroreflex-mediated sympathetic AP regulation and also spares the magnitude of the sympathetic HR response, despite significant bradycardia. The preserved sympathetic HR response, which could not be afforded by beta-blockers, may contribute to some beneficial clinical effects of ivabradine.