Sugammadex sodium (Org25969) , a synthetic derivative of γ-cyclodextrin, is a steroid-based neuromuscular blocker reversing agent.

注射100 ug/kg 的罗库溴铵可以实现平均93.0%的神经肌肉阻滞，而通过注射500 ug/kg 的剂量可以达到深度阻滞。在注射高剂量罗库溴铵后，四连征比率90%的恢复时间分别为：使用生理盐水后28分钟，使用1 mg/kg sugammadex后26分钟，使用2.5 mg/kg sugammadex后缩短至8分钟。在此过程中，没有观察到残留阻滞或再次阻滞的迹象[1]。在短暂全脑缺血/再灌注（I/R）大鼠模型中，16 mg/kg与100 mg/kg sugammadex的治疗表现出神经保护作用，但100 mg/kg的sugammadex对大鼠具有更显著的神经保护效果[2]。

The animals were anesthetized with 80 mg/kg ketamine hydrochloride and 12 mg/kg xylazine administered intraperitoneally. After the rats were anesthetized, the bilateral common carotid arteries were exposed and carefully separated from the carotid sheath and the cervical sympathetic and vagal nerves through a ventral cervical incision. The bilateral common carotid arteries were occluded with nontraumatic aneurysm clips in ischemic rats but were not clamped in sham-operated rats. Complete interruption of the blood flow was confirmed by observing the central artery in the retina with an ophthalmoscope. The body temperature of the rats was maintained at 37.0 ± 0.5°C during this procedure. In this model, 10 minutes of ischemia and 24 hours of reperfusion were induced. After the ischemic period, the rats were treated with sugammadex 16 mg/kg (S 16 group) and sugammadex 100 mg/kg (S 100 group) (intravenous and total volume 1 mL) in the 5th minute of reperfusion. Sugammadex was diluted with normal saline (0.9% NaCl). The same surgical procedure was performed in the I/R group, but the rats were not treated with sugammadex. The neck incision was closed with sutures (3.0 silk), and the animals were allowed to awaken. After 24 hours, the neurological condition of the rats was assessed with a scoring system [2].