Herman-Gnjidic Z, MacLusky N J, Lye S J
Division of Perinatology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
Am J Obstet Gynecol. 1994 Dec;171(6):1651-9. doi: 10.1016/0002-9378(94)90417-0.
Our purpose was to determine the ability of dexamethasone to prevent the onset of myometrial desensitization to beta-adrenergic agonists in vivo.
On day 5 post partum chronically catheterized rats were randomized to receive either dexamethasone or corn oil (vehicle), followed 12 hours later by a continuous infusion of either isoproterenol or saline solution (vehicle). Uterine contractions were monitored throughout. We measured myometrial glucocorticoid receptor levels in chronically catheterized and sham-operated rats and beta 2-adrenergic receptor densities in the experimental rats before and during the infusions.
Surgery did not lead to any decrease in glucocorticoid receptor number. Dexamethasone significantly increased the duration of myometrial responsiveness to isoproterenol compared with vehicle-pretreated rats, although agonist-induced down-regulation of beta-adrenergic receptor number was not prevented.
Dexamethasone partially protects the rat myometrium from desensitization induced by the continuous infusion of beta-adrenergic agonists through mechanisms independent of the beta 2-receptor.
我们的目的是确定地塞米松在体内预防子宫肌层对β-肾上腺素能激动剂脱敏的能力。
产后第5天，将长期插管的大鼠随机分为两组，分别接受地塞米松或玉米油（赋形剂），12小时后，再分别持续输注异丙肾上腺素或盐溶液（赋形剂）。全程监测子宫收缩情况。我们在长期插管大鼠和假手术大鼠中测量子宫肌层糖皮质激素受体水平，并在输注前及输注过程中测量实验大鼠的β2-肾上腺素能受体密度。
手术并未导致糖皮质激素受体数量减少。与接受赋形剂预处理的大鼠相比，地塞米松显著延长了子宫肌层对异丙肾上腺素的反应持续时间，尽管激动剂诱导的β-肾上腺素能受体数量下调未得到预防。
地塞米松通过独立于β2受体的机制部分保护大鼠子宫肌层免受持续输注β-肾上腺素能激动剂诱导的脱敏作用。
