Pourcyrous M, Leffler C W, Bada H S, Korones S B, Stidham G L, Busija D W
Department of Pediatrics, University of Tennessee, Memphis 38163.
Pediatr Res. 1992 Jun;31(6):636-9. doi: 10.1203/00006450-199206000-00019.
We investigated the effects of pancuronium bromide pretreatment on cerebral blood flow (CBF) during bicuculline-induced seizures in anesthetized piglets. Arterial blood pressure, gases, pH, cerebral electrocortical activity, and CBF (radioactive microsphere) were monitored at baseline, 10 min after administration of pancuronium (0.3 mg/kg i.v.; n = 9) or vehicle (normal saline; n = 8), and again at 5, 15, and 60 min after bicuculline (3 mg/kg i.v.). No change in CBF from baseline was observed at 10 min after either saline or pancuronium treatment, before induction of seizures. In the saline group, CBF was 36 +/- 3 mL.min-1.100 g-1 before bicuculline and increased to 166 +/- 24 and 205 +/- 35 mL.min-1.100 g-1 at 5 and 15 min, respectively, after bicuculline, returning toward baseline by 60 min. In the pancuronium group at 5 min after bicuculline, CBF increased from 45 +/- 7 to 169 +/- 26 mL.min-1.100 g-1, but fell to 88 +/- 17 mL.min-1.100 g-1 at 15 min in contrast to saline-treated piglets. Also, at 15 min of seizures, differences between groups were observed in arterial blood pressure, gases, and pH. Although these variables were in the normal range with pancuronium treatment, the saline-treated animals had increased arterial blood pressure (81 +/- 6 mm Hg) and PCO2 (6 +/- 0.4 kPa) and decreased PO2 (7 +/- 0.5 kPa) and pH (6.91 +/- 0.06). Electrocortical activity was abnormal during seizures in both groups. At 60 min, reversal to normal activity was observed in six of nine pancuronium-treated animals versus two of eight saline-treated animals. These data suggest that pancuronium limits cerebral hyperemia during prolonged seizures by attenuating increases in blood pressure as a result of elimination of skeletal muscle activity. This leads to minimal alteration of arterial PCO2, PO2, and pH during seizures.
我们研究了泮库溴铵预处理对麻醉仔猪荷包牡丹碱诱发癫痫发作期间脑血流量（CBF）的影响。在基线、静脉注射泮库溴铵（0.3mg/kg；n = 9）或赋形剂（生理盐水；n = 8）10分钟后，以及静脉注射荷包牡丹碱（3mg/kg）5、15和60分钟后，监测动脉血压、气体、pH值、大脑皮层电活动和CBF（放射性微球）。在癫痫发作诱导前，生理盐水或泮库溴铵治疗10分钟后，CBF与基线相比无变化。在生理盐水组，荷包牡丹碱注射前CBF为36±3mL·min⁻¹·100g⁻¹，注射后5分钟和15分钟分别增加至166±24和205±35mL·min⁻¹·100g⁻¹，60分钟时恢复至基线水平。在泮库溴铵组，荷包牡丹碱注射后5分钟，CBF从45±7增加至169±26mL·min⁻¹·100g⁻¹，但与生理盐水处理的仔猪相比，15分钟时降至88±17mL·min⁻¹·100g⁻¹。此外，在癫痫发作15分钟时，观察到两组在动脉血压、气体和pH值方面存在差异。尽管泮库溴铵治疗时这些变量在正常范围内，但生理盐水处理的动物动脉血压（81±6mmHg）和PCO₂（6±0.4kPa）升高，PO₂（7±0.5kPa）和pH值（6.91±0.06）降低。两组癫痫发作期间大脑皮层电活动均异常。60分钟时，9只泮库溴铵治疗的动物中有6只恢复正常活动，而8只生理盐水治疗的动物中有2只恢复正常活动。这些数据表明，泮库溴铵通过减弱因骨骼肌活动消除导致的血压升高，限制长时间癫痫发作期间的脑充血。这导致癫痫发作期间动脉PCO₂、PO₂和pH值的变化最小。
