Aviation, space, and environmental medicine · 2005
Cerebral hypoperfusion precedes nausea during centrifugation.
СтатьяПоддержка правительства СШАПоддержка службы здравоохранения СШАНазвание 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.
Serrador Jorge M, Schlegel Todd T, Black F Owen, Wood Scott J, New Collective Author
Аннотация
INTRODUCTION: Nausea and motion sickness are important operational concerns for aviators and astronauts. Understanding the underlying mechanisms associated with motion sickness may lead to new treatments. The goal of this work was to determine if changes in cerebral blood flow precede the development of nausea in subjects susceptible to motion sickness.
METHODS: Cerebral flow velocity in the middle cerebral artery (transcranial Doppler), BP, and end-tidal CO2 were measured while subjects were rotated on a centrifuge (250 degrees x s(-1)). Following 5 min of rotation, subjects were translated 51.5 cm off-center, creating a +1 Gx centripetal acceleration in the nasal-occipital plane.
RESULTS: There were 10 subjects who completed the protocol without symptoms while 5 developed nausea (4 while off-center and 1 while rotating on-center). Prior to nausea, subjects had significant increases in BP (+13 +/- 3 mmHg, p < 0.05) and cerebrovascular resistance (+46 +/- 17%, p < 0.05) and decreases in cerebral flow velocity both in the second (-13 +/- 4%) and last minute (-22 +/- 5%) before symptoms (p < 0.05). In comparison, subjects resistant to motion sickness demonstrated no change in BP or cerebrovascular resistance in the last minute of off-center rotation and only a 7 +/- 2% decrease in cerebral flow velocity. All subjects had significant hypocapnia (-3.8 +/- 0.4 mmHg, p < 0.05); however, this hypocapnia could not fully explain the cerebral hypoperfusion associated with the development of nausea.
CONCLUSIONS: These data indicate that reductions in cerebral blood flow precede the development of nausea. Further work is necessary to determine what role cerebral hypoperfusion plays in motion sickness and whether cerebral hypoperfusion can be used to predict the development of nausea in susceptible individuals.
METHODS: Cerebral flow velocity in the middle cerebral artery (transcranial Doppler), BP, and end-tidal CO2 were measured while subjects were rotated on a centrifuge (250 degrees x s(-1)). Following 5 min of rotation, subjects were translated 51.5 cm off-center, creating a +1 Gx centripetal acceleration in the nasal-occipital plane.
RESULTS: There were 10 subjects who completed the protocol without symptoms while 5 developed nausea (4 while off-center and 1 while rotating on-center). Prior to nausea, subjects had significant increases in BP (+13 +/- 3 mmHg, p < 0.05) and cerebrovascular resistance (+46 +/- 17%, p < 0.05) and decreases in cerebral flow velocity both in the second (-13 +/- 4%) and last minute (-22 +/- 5%) before symptoms (p < 0.05). In comparison, subjects resistant to motion sickness demonstrated no change in BP or cerebrovascular resistance in the last minute of off-center rotation and only a 7 +/- 2% decrease in cerebral flow velocity. All subjects had significant hypocapnia (-3.8 +/- 0.4 mmHg, p < 0.05); however, this hypocapnia could not fully explain the cerebral hypoperfusion associated with the development of nausea.
CONCLUSIONS: These data indicate that reductions in cerebral blood flow precede the development of nausea. Further work is necessary to determine what role cerebral hypoperfusion plays in motion sickness and whether cerebral hypoperfusion can be used to predict the development of nausea in susceptible individuals.