COCAINE EFFECTS ON CNS-RELATED CARDIORESPIRATORY CONTROL

这些研究的目的是检查中枢神经控制 呼吸和心脏模式的影响 自由活动的猫。 这一目标是基于 可卡因改变边缘系统活动的假设 通常对心脏有影响的结构 呼吸模式，以及可卡因给药导致的死亡， 可能是由于CNS对上气道的影响， 肌肉系统，或来自心脏的中枢作用 节律，也许由外周血管收缩或 可卡因引起的体温过高可卡因的剂量反应将是 与上呼吸道肌肉组织的模式相关进行评估 和横膈膜，以及血压，心率， 心律不齐 EEG和单神经元放电将在 边缘系统和脑干结构， 在心血管和呼吸模式中起作用。 这些 结构包括杏仁核的中央核， 脑桥臂旁内侧肌，孤束核 束和舌下神经核。 肌电活动 包括环杓后肌在内的上气道肌肉 主要喉扩张肌和甲杓肌 肌肉，喉缩肌，将被记录，连同 肋膈的活动。 动脉压将 从留置颈动脉插管记录，并将ECG 从脑电肌电图导联采集的信号 核心和前部 下丘脑温度将被监测， themprobes。 低、中、高剂量可卡因或对照 将静脉注射生理盐水，电生理活动将 记录交货后24小时。 脑桥和杏仁核部位 会被可卡因冷却后可逆性地阻断 行政当局审查这些结构在调解 心脏和呼吸系统的影响。 数据将被写入 测谎仪，在PDP 11/73计算机上数字化，并使用 关于剂量相关1）吸气和呼气时间 上呼吸道和横膈膜的改变，2） 上呼吸道，3）隔膜的呼吸暂停或呼吸暂停活动， 4)阶段性或紧张性动脉压的改变，5）心脏 心律失常，6）高热，7）激活EMG或癫痫放电 在边缘系统和脑干区域，以及8）与大脑相关的单个 边缘系统和脑干区的神经元放电。

The objective of these studies is to examine central neural control over respiratory and cardiac patterning following acute cocaine administration in freely moving cats. This objective is based on the assumption that cocaine alters activity in limbic system structures which normally have an influence on cardiac and respiratory patterning, and that death from cocaine administration may result from CNS effects on either the upper airway or diaphragmatic musculature, or from central effects on cardiac rhythms, perhaps compounded by peripheral vasoconstriction or hyperthermia induced by cocaine Dose-responses of cocaine will be assessed in relation to patterning of the upper airway musculature and the diaphragm, as well as to blood pressure, heart rate, and arrhythmias. EEG and single-neuron discharge will be examined in limbic and brainstem structures while have been demonstrated to have roles in cardiovascular and respiratory patterning. These structures include the central nucleus of the amygdala, the nucleus parabrachialis medialis of the pons, the nucleus of the solitary tract, and the hypoglossal nucleus. Electromyograhic activity of upper airway muscles including the posterior cricoarytenoid muscles, the major laryngeal dilator, and the thyroarytenoid muscle, a laryngeal constrictor, will be recorded, together with activity of the costal diaphragm. Arterial pressure will be recorded from an indwelling carotid cannula, and the ECG will be acquired from the diaphragmatic EMG leads. Core and anterior hypothalamic temperature will be monitored with miniaturized themprobes. Low, medium, and high doses of cocaine or control saline will be injected IV, and electrophysiological activity will be recorded for 24 hr post delivery. Pontine and amygdala sites will be reversibly blockaded by cooling following cocaine administration to examine the role of these structures in mediating cardiac and respiratory effects. Data will be written on a polygraph, digitized on a PDP 11/73 computer, and analyzed with respect to dose-related 1) inspiratory and expiratory timing alterations in the upper airway and diaphragm, 2) obstruction of the upper airway, 3) apneustic or apneic activity of the diaphragm, 4) alterations in phasic or tonic arterial pressure, 5) cardiac arrhythmias, 6) hyperpyrexia, 7) activated EMG or seizure discharge in limbic and brainstem areas, and 8) respiratory-related single neuron discharge in limbic and brainstem areas.