Farber N E, Schmidt J E, Kampine J P, Schmeling W T
Department of Anesthesiology, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee 53226, USA.
Anesthesiology. 1995 Dec;83(6):1241-53. doi: 10.1097/00000542-199512000-00015.
In vivo, halothane alters spontaneous firing in and thermosensitivity of neurons in the preoptic region of the anterior hypothalamus. To better understand the mechanisms by which halothane specifically disrupts normal thermoregulation, this investigation examined the effects of halothane on thermosensitive preoptic region neurons in isolated hypothalamic tissue slices.
Brain slices were obtained and prepared from Sprague-Dawley rats. Preoptic region neurons were characterized by extracellular recording of spontaneous firing rates and thermosensitivity to localized heating and cooling, before, during, and after halothane equilibrated in the perfusate and carrier gas.
One hundred sixteen neurons were characterized by their thermosensitivity as: 29% warm-sensitive (> 0.8 spikes.s-1.degrees C-1); 14% cold-sensitive (< 0.6 spikes.s-1.degrees C-1); and 57% temperature-insensitive. Halothane significantly reduced the spontaneous firing rates to 64% of control and the thermosensitivity to 55% of control for warm-sensitive neurons at 1% halothane. Halothane significantly reduced the spontaneous firing rate of cold-sensitive neurons to 24 and 40% of control, and the thermosensitivity to 61 and 36% of control at 0.5, and 1% halothane, respectively. Spontaneous firing rates and thermosensitivity returned toward control values in warm-sensitive neurons (92 and 122% of control, respectively) after discontinuation of halothane, which did not occur in cold-sensitive neurons (49 and 36% of control, respectively). Halothane did not alter the thermosensitive temperature range or the set point temperature at which neurons became most thermosensitive. Halothane also did not affect the firing rates of temperature-insensitive neurons.
Halothane alters the firing rate and thermosensitivity of individual temperature-sensitive neurons in in vitro slices of the preoptic region of the anterior hypothalamus in the absence of afferent modulation. This disruption may result in an imprecision of thermoregulatory responses locally within the preoptic region, to thermal challenges and represents a potential mechanism by which halothane widens the thermoregulatory threshold range.
在体内，氟烷会改变下丘脑前部视前区神经元的自发放电和热敏性。为了更好地理解氟烷特异性破坏正常体温调节的机制，本研究考察了氟烷对离体下丘脑组织切片中热敏视前区神经元的影响。
从Sprague-Dawley大鼠获取并制备脑切片。在灌注液和载气中平衡氟烷之前、期间和之后，通过细胞外记录自发放电率以及对局部加热和冷却的热敏性来对视前区神经元进行特征描述。
116个神经元根据其热敏性分为：29%为温敏型（>0.8个脉冲·秒⁻¹·℃⁻¹）；14%为冷敏型（<0.6个脉冲·秒⁻¹·℃⁻¹）；57%为温度不敏感型。在1%氟烷浓度下，氟烷显著降低了温敏型神经元的自发放电率至对照值的64%，热敏性至对照值的55%。在0.5%和1%氟烷浓度下，氟烷分别显著降低了冷敏型神经元的自发放电率至对照值的24%和40%，热敏性至对照值的61%和36%。在停止使用氟烷后，温敏型神经元的自发放电率和热敏性恢复至对照值（分别为对照值的92%和122%），而冷敏型神经元则未恢复（分别为对照值的49%和36%）。氟烷未改变热敏温度范围或神经元最敏感时的设定点温度。氟烷也未影响温度不敏感型神经元的放电率。
在无传入调节的情况下，氟烷改变了下丘脑前部视前区体外切片中单个温度敏感型神经元的放电率和热敏性。这种破坏可能导致视前区内局部体温调节反应对热刺激的不精确性，这代表了氟烷拓宽体温调节阈值范围的一种潜在机制。
