Bonvento G, Charbonné R, Corrèze J L, Borredon J, Seylaz J, Lacombe P
Laboratoire de Recherches Cérébrovasculaires, CNRS UA 641, Faculté de Médecine Lariboisière-Saint Louis, Université Paris, VII France.
Brain Res. 1994 Dec 5;665(2):213-21. doi: 10.1016/0006-8993(94)91340-4.
The aim of this study was to determine whether alpha-chloralose, when associated with an initial period of halothane, is a suitable anesthetic regimen for cerebrovascular studies. For this purpose, rats anesthetized with alpha-chloralose plus halothane induction were first subjected to noxious stimuli, and the behavior, EEG and systemic variables were recorded. During a second step, cortical blood flow was measured with laser-Doppler flowmetry and the time-course of the cerebrovascular reactivity to hypercapnia were measured in artificially ventilated rats anesthetized with either alpha-chloralose (40 mg.kg-1, s.c.) plus halothane induction (1.5% given during the first 45-60 min) or halothane alone (1.5%). Finally, an experimental paradigm was developed that allowed the comparison of the hypercapnic reactivity, both in awake and anesthetized conditions in the same animal. Our results show that the association of alpha-chloralose with halothane leads to stable cardiovascular parameters and immobility of ventilated rats, placed in ear bars without curare, for 3 h without any sign of discomfort. Based on EEG criteria, we found that halothane induction lengthens the duration of alpha-chloralose anesthesia (253 +/- 19 vs. 200 +/- 15 min, P < 0.01). Under alpha-chloralose alone or in association with halothane induction, the vascular reactivity to hypercapnia was considerably impaired (-85% compared to the awake state, P < 0.01), but this impairment was transient, since a control reactivity was restored 150-190 min after induction of anesthesia. Under halothane alone, the vascular reactivity remained reduced throughout the experiment. These results provide evidence that alpha-chloralose plus halothane induction is a suitable anesthetic regimen which displays a temporal window of normal cerebrovascular reactivity.
本研究的目的是确定与初始阶段的氟烷联合使用时,α-氯醛糖是否是适合脑血管研究的麻醉方案。为此,对用α-氯醛糖加氟烷诱导麻醉的大鼠首先施加有害刺激,并记录其行为、脑电图和全身变量。在第二步中,用激光多普勒血流仪测量皮质血流量,并在人工通气的大鼠中测量对高碳酸血症的脑血管反应性的时间进程,这些大鼠分别用α-氯醛糖(40mg·kg-1,皮下注射)加氟烷诱导(在最初45-60分钟内给予1.5%)或单独使用氟烷(1.5%)麻醉。最后,建立了一种实验范式,可在同一动物的清醒和麻醉条件下比较高碳酸血症反应性。我们的结果表明,α-氯醛糖与氟烷联合使用可使心血管参数稳定,且在不使用箭毒的情况下置于耳杆中的通气大鼠可保持3小时不动,无任何不适迹象。根据脑电图标准,我们发现氟烷诱导延长了α-氯醛糖麻醉的持续时间(253±19分钟对200±15分钟,P<0.01)。单独使用α-氯醛糖或与氟烷诱导联合使用时,对高碳酸血症的血管反应性显著受损(与清醒状态相比降低85%,P<0.01),但这种损害是短暂的,因为在麻醉诱导后150-190分钟恢复了对照反应性。单独使用氟烷时,整个实验过程中血管反应性仍然降低。这些结果证明,α-氯醛糖加氟烷诱导是一种合适的麻醉方案,其显示出正常脑血管反应性的时间窗。