七氟醚麻醉大鼠脑钠泵活性的动态变化

目的 :动态观察七氟醚吸入麻醉不同时期大鼠各脑区Na+ ,K+ -ATP酶活性变化 ,结合行为学改变 ,探讨七氟醚麻醉的作用机制。方法 :4 0只SD大鼠随机均分为 5组 :对照组、诱导期组、麻醉期组、恢复期组和清醒期组。用分光光度法测定不同时期大脑皮层、脑干、海马Na+ ,K+ -ATP酶活性变化。结果 :大鼠各脑区Na+ ,K+ -ATP酶活性在诱导期即开始下降 ,大脑皮层、脑干、海马Na+ ,K+ -ATP酶活性分别降低 2 1.9%、10 .5 %、19.3% ,其中大脑皮层和海马Na+ ,K+ -ATP酶活性的降低有统计学意义 (与对照组比较 ,P <0 .0 5 ) ;麻醉期Na+ ,K+ -ATP酶活性下降至最低 (P <0 .0 1) ,大脑皮层、脑干、海马Na+ ,K+ -ATP酶活性分别降低 37.2 %、33.5 %、38.9% ;恢复期Na+ ,K+ -ATP酶活性又开始升高 ,但仍低于对照组水平 (P <0 .0 5或P <0 .0 1) ,大脑皮层、脑干、海马Na+ ,K+ -ATP酶活性分别降低 18.3%、17.9% (P <0 .0 5 )和 2 2 .6 % (P <0 .0 1) ;而清醒期该酶活性基本恢复至对照组水平 (P >0 .0 5 )。大鼠各脑区Na+ ,K+ -ATP酶活性改变与麻醉深度的变化相平行。结论 :七氟醚可明显抑制大鼠大脑皮层、脑干、海马Na+ ,K+ -ATP酶活性 ,且与行为变化相平行 ,提示七氟醚可能通过抑制Na+ ,K+ -ATP酶活性而发挥麻醉效应 ,麻醉深度与?

The dynamic change of Na+,K+-ATPase activity in rat brain at different stages of sevoflurane anesthesia

Objective To determine the effect of sevoflurane on Na +,K +-ATPase activity in different brain regions of rat at different anesthesia stages and explore the anesthetic mechanism of sevoflurane. Methods Forty rats weighing 250～300 g were randomly divided into five groups of 8 animals each, group 1:control; group 2: induction of anesthesia; group 3: maintenance of anesthesia; group 4: recovery from anesthesia and group 5: complete recovery. Rats were placed in a special glass anesthesia box and exposed to 2.5% sevoflurane. The induction of anesthesia started from staggering of the animal to loss of righting reflex, maintenance of anesthesia from 1min after loss of righting reflex, recovery of anesthesia from recovery of righting reflex to staggering after sevoflurane anesthesia was discontinued and glass box was opened and complete recovery from 1h after recovery of righting reflex. The animals were decapitated at different stages of anesthesia. Cerebral cortex, hippocampus and brain stem were immediately removed on ice and frozen in liquid nitrogen. The Na +,K +-ATPase activity in different brain regions of rat at different anesthesia stages were measured by spectroscopic analysis. Results The Na +,K +-ATPase activity in cerebral cortex, brain stem and hippocampus begun to decrease during the induction of anesthesia and reached the lowest level during maintenance of anesthesia, began to increase during recovery from anesthesia and returned to preanesthetic level during complete recovery. Conclusion Sevoflurane significantly inhibits the Na +,K +-ATPase activity in the brain, which is closely related to the depth of anesthesia. Our data suggest that Na +,K +-ATPase in central nervous system may be involved in the mechanism of sevoflurane anesthesia.