Gaudy J H, Sicard J F, Maneglia R, Quignon M
Laboratoire d'Anesthésiologie, Faculté de Médecine Saint-Antoine, Paris, France.
Can J Anaesth. 1993 Sep;40(9):883-90. doi: 10.1007/BF03009263.
Halothane decreases the ventilatory response to hypoxia and the activity of peripheral arterial chemoreceptors, resulting in "chemical chemodenervation." In order to evaluate the role of this halothane-induced "chemical denervation" in acid-base and arterial blood gas changes, these values were measured in intact and chemodenervated rats, awake and under anaesthesia. Since the depth of anaesthesia could be modified by the anatomical chemodenervation, the ED50 of inspired halothane was determined in six rats before and after anatomical chemodenervation. To prevent haemodynamic changes due to halothane and/or anatomical chemodenervation from interfering with the results, systemic arterial blood pressure and heart rate were measured in six intact rats, awake and then anaesthetized, and in the same rats after chemodenervation, awake and then anaesthetized. In nine intact rats and in 19 chemodenervated rats, arterial pH, arterial bicarbonate concentration, and arterial blood gases (PaO2 and PaCO2) were measured before and after administration of halothane. Anatomical chemodenervation modified neither the inspired ED50 (1.1%), nor the mean arterial blood pressure or heart rate. The haemodynamic effects of halothane were comparable in intact and in chemodenervated rats. Changes in arterial blood gases and acid-base balance due to halothane in intact rats and due to chemodenervation in awake rats were not different, but there was a decrease in PaO2 and pHa, and an increase in PaCO2. In chemodenervated rats, halothane caused a further decrease in PaO2 and a further increase in PaCO2. The fact that halothane and anatomical chemodenervation have similar effects on arterial blood gases and acid-base balance favours a "chemical chemodenervating" action of halothane. However, the additional effects of halothane in the anatomically chemodenervated animal show that the action of halothane on blood gases and acid-base balance is the result of multiple sites of impact on the respiratory system.
氟烷会降低对低氧的通气反应以及外周动脉化学感受器的活性,从而导致“化学性化学去神经支配”。为了评估这种氟烷诱导的“化学去神经支配”在酸碱和动脉血气变化中的作用,在完整和化学去神经支配的大鼠中,分别在清醒和麻醉状态下测量了这些数值。由于麻醉深度可通过解剖学去神经支配进行改变,因此在解剖学去神经支配前后,对六只大鼠测定了吸入氟烷的半数有效剂量(ED50)。为防止氟烷和/或解剖学去神经支配引起的血流动力学变化干扰结果,在六只完整大鼠中,分别在清醒和麻醉状态下测量了全身动脉血压和心率,并且在这些大鼠进行化学去神经支配后,同样在清醒和麻醉状态下进行了测量。在九只完整大鼠和十九只化学去神经支配的大鼠中,在给予氟烷前后测量了动脉pH值、动脉碳酸氢盐浓度以及动脉血气(动脉血氧分压[PaO2]和动脉血二氧化碳分压[PaCO2])。解剖学去神经支配既未改变吸入ED50(1.1%),也未改变平均动脉血压或心率。氟烷对完整大鼠和化学去神经支配大鼠的血流动力学影响相当。完整大鼠中由氟烷引起的动脉血气和酸碱平衡变化与清醒大鼠中由化学去神经支配引起的变化并无差异,但动脉血氧分压(PaO2)和动脉血pH值(pHa)下降,动脉血二氧化碳分压(PaCO2)升高。在化学去神经支配的大鼠中,氟烷导致动脉血氧分压(PaO2)进一步下降,动脉血二氧化碳分压(PaCO2)进一步升高。氟烷和解剖学去神经支配对动脉血气和酸碱平衡具有相似作用这一事实,支持了氟烷的“化学性化学去神经支配”作用。然而,氟烷在解剖学去神经支配动物中的额外作用表明,氟烷对血气和酸碱平衡的作用是对呼吸系统多个作用位点产生影响的结果。