Hoffman W E, Baughman V L, Albrecht R F
Department of Anesthesiology, University of Illinois College of Medicine, Chicago.
Anesth Analg. 1993 Nov;77(5):908-12. doi: 10.1213/00000539-199311000-00006.
The interaction of plasma catecholamines and nitrous oxide (N2O) ventilation was examined during brain ischemia in rats. Group 1 (n = 19) was anesthetized with 50 micrograms.kg-1 x h-1 of fentanyl and ventilated with 70% nitrogen in oxygen. Group 2 (n = 19) was anesthetized with intravenous fentanyl (25 micrograms.kg-1 x h-1) and 70% N2O ventilation in oxygen. Group 3 (n = 10) received 25 micrograms.kg-1 x h-1 of fentanyl and 70% N2O ventilation and 100 micrograms/kg of dexmedetomidine, an alpha 2-adrenergic receptor agonist that decreases sympathetic activity. Incomplete brain ischemia was produced by right carotid ligation combined with hemorrhagic hypotension to 30 mm Hg for 30 min. Plasma catecholamines were measured during ischemia. Cerebral blood flow (CBF) was evaluated by using laser Doppler. Neurologic outcome was evaluated for 3 days after ischemia. Plasma epinephrine and norepinephrine and were decreased 20% and neurologic outcome was significantly worse in Group 2 ventilated with N2O compared with fentanyl-anesthetized controls (P < 0.05). Dexmedetomidine-treated rats had lower plasma catecholamines (20% of control) and larger decreases in CBF during ischemia compared with controls. Dexmedetomidine (Group 3) improved outcome from ischemia in comparison to both Groups 1 and 2 (P < 0.05). These results suggest that catecholamines play a major role in worsening ischemic outcome. N2O ventilation may increase neuronal injury by enhancing the sympathetic response to ischemia.
在大鼠脑缺血期间，研究了血浆儿茶酚胺与一氧化二氮（N₂O）通气之间的相互作用。第1组（n = 19）用50微克·千克⁻¹·小时⁻¹的芬太尼麻醉，并用70%的氮气-氧气混合气通气。第2组（n = 19）用静脉注射芬太尼（25微克·千克⁻¹·小时⁻¹）和70%的N₂O-氧气混合气通气。第3组（n = 10）接受25微克·千克⁻¹·小时⁻¹的芬太尼、70%的N₂O通气以及100微克/千克的右美托咪定，右美托咪定是一种可降低交感神经活性的α₂肾上腺素能受体激动剂。通过右侧颈动脉结扎并将出血性低血压降至30毫米汞柱持续30分钟来造成不完全性脑缺血。在缺血期间测量血浆儿茶酚胺。使用激光多普勒评估脑血流量（CBF）。在缺血后3天评估神经功能结局。与芬太尼麻醉的对照组相比，第2组用N₂O通气时血浆肾上腺素和去甲肾上腺素降低了20%，且神经功能结局明显更差（P < 0.05）。与对照组相比，右美托咪定治疗的大鼠血浆儿茶酚胺水平较低（为对照组的20%），且在缺血期间CBF的降低幅度更大。与第１组和第2组相比，右美托咪定（第3组）改善了缺血后的结局（P < 0.05）。这些结果表明，儿茶酚胺在使缺血结局恶化中起主要作用。N₂O通气可能通过增强对缺血的交感反应而增加神经元损伤。
