American journal of obstetrics and gynecology · 1996
Cocaine and beta-adrenergic receptor function in pregnant myometrium.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения 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.
Wang F L, Dombrowski M P, Hurd W W
Аннотация
OBJECTIVE: Our purpose was to evaluate the in vitro effect of cocaine on beta-adrenergic receptor function in pregnant human myometrium.
STUDY DESIGN: Myometrium was obtained from 25 pregnant women at term who were undergoing cesarean section but who were not in labor. Membrane preparations were assayed for cyclic adenosine monophosphate production after exposure to isoproterenol, sodium fluoride, or forskolin in the presence and absence of either cocaine or benzoylecgonine, a major metabolite of cocaine.
RESULTS: Cocaine inhibited isoproterenol-induced cyclic adenosine monophosphate production in concentrations as low as 10(-8) mol/L but had no effect on cyclic adenosine monophosphate production induced by sodium fluoride or forskolin. Benzoylecgonine (10(-4) mol/L) had no effect on isoproterenol-induced cyclic adenosine monophosphate production.
CONCLUSION: Cocaine is a beta-adrenergic receptor antagonist in human myometrium at concentrations as low as 10(-8) mol/L. This acute effect of cocaine may result in increased uterine contractility with adrenergic stimulation, potentially leading to increased uterine activity associated with acute cocaine use.
STUDY DESIGN: Myometrium was obtained from 25 pregnant women at term who were undergoing cesarean section but who were not in labor. Membrane preparations were assayed for cyclic adenosine monophosphate production after exposure to isoproterenol, sodium fluoride, or forskolin in the presence and absence of either cocaine or benzoylecgonine, a major metabolite of cocaine.
RESULTS: Cocaine inhibited isoproterenol-induced cyclic adenosine monophosphate production in concentrations as low as 10(-8) mol/L but had no effect on cyclic adenosine monophosphate production induced by sodium fluoride or forskolin. Benzoylecgonine (10(-4) mol/L) had no effect on isoproterenol-induced cyclic adenosine monophosphate production.
CONCLUSION: Cocaine is a beta-adrenergic receptor antagonist in human myometrium at concentrations as low as 10(-8) mol/L. This acute effect of cocaine may result in increased uterine contractility with adrenergic stimulation, potentially leading to increased uterine activity associated with acute cocaine use.