Shu C C, Hoffman W E, Thomas C, Albrecht R F
Department of Anesthesiology, University of Illinois, Chicago.
Anesthesiology. 1993 Jun;78(6):1120-5. doi: 10.1097/00000542-199306000-00015.
Studies have shown that increased sympathetic activity or increased blood and brain glucose concentration worsen postischemic brain damage. The authors evaluated the interaction of plasma glucose with epinephrine and norepinephrine during incomplete cerebral ischemia in the rat using ganglionic blockade.
Rats were anesthetized with 25 micrograms.kg-1.h-1 fentanyl and 70% nitrous oxide in oxygen. Ganglionic blockade was produced in 30 rats using 8 mg/kg hexamethonium intravenously. Three plasma glucose ranges, low < 150 mg/dl, moderate = 150-300 mg/dl, and high > 300 mg/dl, were produced in each group. Ischemia was induced by unilateral carotid ligation and hemorrhagic hypotension to 30 mmHg for 30 min. Plasma norepinephrine and epinephrine were measured by radioimmunoassay. Neurologic outcome was evaluated daily for 3 days after ischemia.
Ganglionic blockade decreased blood pressure before the start of ischemia and plasma epinephrine and norepinephrine during ischemia (P < 0.05). Neurologic outcome was significantly worse in rats with high glucose compared with low glucose concentrations with and without ganglionic blockade (P < 0.05). Neurologic outcome and stroke-related mortality were worse in rats with increased plasma epinephrine and norepinephrine compared with rats with ganglionic blockade when plasma glucose was less than 300 mg/dl (P < 0.05).
These results indicate that increased concentration of catecholamines enhance glucose-related injury during incomplete ischemia in rats.
研究表明，交感神经活动增加或血液及脑葡萄糖浓度升高会加重缺血后脑损伤。作者利用神经节阻断法评估了大鼠不完全性脑缺血期间血浆葡萄糖与肾上腺素和去甲肾上腺素之间的相互作用。
用25微克·千克⁻¹·小时⁻¹的芬太尼和70%氧化亚氮与氧气混合麻醉大鼠。30只大鼠静脉注射8毫克/千克六甲铵以产生神经节阻断。每组设定三个血浆葡萄糖范围，低<150毫克/分升、中=150 - 300毫克/分升、高>300毫克/分升。通过单侧颈动脉结扎和出血性低血压使血压降至30毫米汞柱并维持30分钟来诱导缺血。采用放射免疫分析法测定血浆去甲肾上腺素和肾上腺素。缺血后3天每天评估神经功能结局。
神经节阻断使缺血开始前的血压以及缺血期间的血浆肾上腺素和去甲肾上腺素降低（P<0.05）。无论有无神经节阻断，高血糖大鼠的神经功能结局均显著差于低血糖大鼠（P<0.05）。当血浆葡萄糖低于300毫克/分升时，血浆肾上腺素和去甲肾上腺素升高的大鼠与有神经节阻断的大鼠相比，神经功能结局及卒中相关死亡率更差（P<0.05）。
这些结果表明，儿茶酚胺浓度升高会增强大鼠不完全缺血期间与葡萄糖相关的损伤。
