Aviation, space, and environmental medicine · 2003
Baroreflex control of heart rate during heating in subjects with low orthostatic tolerance.
СтатьяПоддержка 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.
Yamazaki Fumio, Kawahara Chie, Soga Izumi, Yamada Shinwa, Hamasaki Kunshige
Аннотация
BACKGROUND: Heat stress induces a reduction of orthostatic tolerance. The cardiovascular responses, including the cardiac baroreflex response to heat stress, were examined to test the hypothesis that subjects with orthostatically low tolerance demonstrate an impaired baroreflex control of heart rate (HR) during heat stress.
METHODS: There were 44 healthy young volunteers who underwent whole body heat stress produced by a hot-water-perfused suit during supine rest for 45 min and 75 degrees head-up tilt (HUT) for 6 min. Esophageal temperature, HR, arterial pressure, and skin blood flow in the forearm and palm were measured continuously throughout the experiment. The sensitivity of the arterial baroreflex control of HR was calculated from the spontaneous changes in beat-to-beat arterial pressure and HR.
RESULTS: The HUT was uneventful for 22 volunteers (higher tolerance group), but 22 volunteers (lower tolerance group) reached presyncope after 195 +/- 19 s. Esophageal temperature, HR, arterial pressure, and skin blood flow changed similarly in the two groups during heating. In the preheating condition, the sensitivity of the baroreflex control of HR did not differ significantly between the two groups. Heating did not alter the sensitivity of baroreflex control of HR in the higher tolerance group, but decreased it significantly in the lower tolerance group. Heating increased the number of heartbeats used for analysis of the baroreflex sensitivity in the higher tolerance group, but did not change it in the lower tolerance group.
CONCLUSIONS: These results suggest that the impairment of vagal baroreflex control of HR during heat exposure aggravates the orthostatic intolerance in heat-stressed humans.
METHODS: There were 44 healthy young volunteers who underwent whole body heat stress produced by a hot-water-perfused suit during supine rest for 45 min and 75 degrees head-up tilt (HUT) for 6 min. Esophageal temperature, HR, arterial pressure, and skin blood flow in the forearm and palm were measured continuously throughout the experiment. The sensitivity of the arterial baroreflex control of HR was calculated from the spontaneous changes in beat-to-beat arterial pressure and HR.
RESULTS: The HUT was uneventful for 22 volunteers (higher tolerance group), but 22 volunteers (lower tolerance group) reached presyncope after 195 +/- 19 s. Esophageal temperature, HR, arterial pressure, and skin blood flow changed similarly in the two groups during heating. In the preheating condition, the sensitivity of the baroreflex control of HR did not differ significantly between the two groups. Heating did not alter the sensitivity of baroreflex control of HR in the higher tolerance group, but decreased it significantly in the lower tolerance group. Heating increased the number of heartbeats used for analysis of the baroreflex sensitivity in the higher tolerance group, but did not change it in the lower tolerance group.
CONCLUSIONS: These results suggest that the impairment of vagal baroreflex control of HR during heat exposure aggravates the orthostatic intolerance in heat-stressed humans.