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首页> 外文期刊>Brain research >Chronic phenytoin treatment reduces rat carotid body chemosensory responses to acute hypoxia
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Chronic phenytoin treatment reduces rat carotid body chemosensory responses to acute hypoxia

机译：慢性苯妥英钠治疗可降低大鼠颈动脉对急性缺氧的化学感应反应

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Ventilation is peripherally controlled by afferent activity arising from the peripheral chemoreceptors. In the rat, chemosensory activity is conveyed to the central nervous system through axons of neurons located in the nodose-petrosal-jugular-complex. These neurons have distinct electrophysiological properties, including a persistent Na+ current. Acute blockade of this current with phenytoin and other anti epileptic drugs reduces normoxic chemosensory activity and responses to acute hypoxia. However, because anti-epileptic therapy is prolonged and there is no information on the effects of chronic phenytoin treatment on peripheral chemosensory activity, we studied the effects of long-lasting phenytoin treatment (similar to 25 days) on afferent chemosensory activity, on a wide range of oxygen inspiratory fractions. Osmotic pumps containing dissolved phenytoin (166 mg/mL) or vehicle (daily flow: 60 mu L) were implanted subcutaneously in male adult Sprague Dawley rats. At the end of the treatment, the animals were anesthetized and carotid sinus nerve activity was recorded in vivo. Afferent chemosensory activity in normoxia was not significantly different between control (71.2 +/- 2.2 Hz) and phenytoin treated (95.4 +/- 2.1 Hz) rats. In contrast, carotid body chemosensory responses to acute hypoxic challenges were markedly reduced in phenytoin treated rats, specifically in the lowest part of the hypoxic range (control 133.5 +/- 18.0 Hz vs phenytoin treated 50.2 +/- 29.4, at 5% F1O2). Chronic phenytoin treatment severely impaired the chemosensory responses to acute hypoxia, suggesting that long-term phenytoin treatment in patients may result in a reduced peripheral respiratory drive together with a reduction in the respiratory responses to hypoxic challenges. (C) 2016 Elsevier B.V. All rights reserved.
机译：通气由周围化学感受器引起的传入活动进行周围控制。在大鼠中，化学感觉活性通过位于结节-岩土-颈静脉复合体中的神经元轴突传递至中枢神经系统。这些神经元具有独特的电生理特性，包括持续的Na +电流。苯妥英钠和其他抗癫痫药对这种电流的急性阻断会降低常氧化学感应活性和对急性缺氧的反应。但是，由于抗癫痫药的治疗时间延长，并且没有关于慢性苯妥英钠治疗对周围化学感觉活性的影响的信息，因此，我们广泛研究了长期苯妥英钠治疗（约25天）对传入化学感应活性的影响吸氧分数范围。将含有溶解的苯妥英（166 mg / mL）或溶媒（日流量：60μL）的渗透泵皮下植入雄性成年Sprague Dawley大鼠中。在治疗结束时，将动物麻醉并在体内记录颈动脉窦神经活动。正常（71.2 +/- 2.2 Hz）和苯妥英治疗（95.4 +/- 2.1 Hz）大鼠之间在正常氧中的传入化学感应活性没有显着差异。相反，在苯妥英钠治疗的大鼠中，特别是在低氧范围的最低部分，对急性低氧挑战的颈动脉体化学感应响应明显降低（在5％F1O2时，对照为133.5 +/- 18.0 Hz，而苯妥英钠为50.2 +/- 29.4 Hz）。 。长期服用苯妥英钠会严重损害对急性缺氧的化学感应反应，这表明长期使用苯妥英钠治疗的患者可能会导致外周呼吸驱动力降低以及对低氧挑战的呼吸反应降低。 （C）2016 Elsevier B.V.保留所有权利。

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