Jugovac Izabela, Imas Olga, Hudetz Anthony G
Department of Anesthesiology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
Anesthesiology. 2006 Oct;105(4):764-78. doi: 10.1097/00000542-200610000-00023.
Anesthetic endpoints of unconsciousness and immobility result from agent effects on both brain and spinal cord that are difficult to separate during systemic administration. To investigate cerebral mechanism of anesthetic-induced unconsciousness, the authors studied behavioral and electrophysiologic effects of four anesthetics infused intracerebroventricularly to conscious rats. The authors aimed to produce progressively increasing anesthetic depths, indicated by electro-encephalographic synchronization and behavioral change.
During anesthesia, rats were equipped with intracerebroventricular infusion catheters, hind-paw stimulation, and epidural electrodes to record the electroencephalogram from the somatosensory cortex. Silicone bolus was injected into the fourth ventricle to minimize drug distribution to the spinal cord. 60 min later, 50-min infusion of pentobarbital (6.0 mg/h), fentanyl (0.75 microg/h), propofol (3.0 mg/h), or midazolam (0.24 mg/h) was initiated. Vibrissal, olfactory, corneal, and tail-pinch responses were tested every 10 min.
All agents depressed vibrissal, olfactory, and corneal responses; propofol and pentobarbital produced the strongest effect. All agents except propofol depressed tail-pinch response; fentanyl and pentobarbital produced the strongest effect. All agents except midazolam increased delta power. Pentobarbital enhanced theta power. All agents except fentanyl enhanced alpha and beta power. Pentobarbital and midazolam slightly increased, whereas fentanyl decreased, gamma power. Pentobarbital increased and midazolam decreased somatosensory evoked potential; these changes were small and apparently unrelated to behavior.
Alpha and beta power increase may reflect sedative component of anesthesia. Simultaneous delta, alpha, and beta power increase may correlate with loss of consciousness. Theta and delta power increase may reflect surgical anesthesia. Opioid-induced gamma power decrease may reflect suppression of pain perception. Pentobarbital-, fentanyl-, and midazolam-induced immobility to noxious stimulation may be mediated supraspinally.
全身给药时,麻醉导致的意识丧失和肌肉松弛这两个终点是由药物对大脑和脊髓的作用引起的,而这两种作用在全身给药过程中很难区分开来。为了研究麻醉诱导意识丧失的脑机制,作者研究了向清醒大鼠脑室内注射四种麻醉药后的行为和电生理效应。作者旨在通过脑电图同步和行为变化来逐步加深麻醉深度。
麻醉期间,给大鼠植入脑室内输注导管、后爪刺激装置和硬膜外电极,以记录体感皮层的脑电图。向第四脑室内注射硅胶团块,以尽量减少药物向脊髓的分布。60分钟后,开始50分钟的戊巴比妥(6.0毫克/小时)、芬太尼(0.75微克/小时)、丙泊酚(3.0毫克/小时)或咪达唑仑(0.24毫克/小时)输注。每隔10分钟测试触须、嗅觉、角膜和夹尾反应。
所有药物均抑制触须、嗅觉和角膜反应;丙泊酚和戊巴比妥的作用最强。除丙泊酚外,所有药物均抑制夹尾反应;芬太尼和戊巴比妥的作用最强。除咪达唑仑外,所有药物均增加δ波功率。戊巴比妥增强θ波功率。除芬太尼外,所有药物均增强α波和β波功率。戊巴比妥和咪达唑仑轻微增加γ波功率,而芬太尼则降低γ波功率。戊巴比妥增加而咪达唑仑降低体感诱发电位;这些变化很小,且显然与行为无关。
α波和β波功率增加可能反映麻醉的镇静成分。δ波、α波和β波功率同时增加可能与意识丧失相关。θ波和δ波功率增加可能反映外科麻醉。阿片类药物引起的γ波功率降低可能反映疼痛感知的抑制。戊巴比妥、芬太尼和咪达唑仑引起的对有害刺激的肌肉松弛可能是由脊髓上机制介导的。