Hogan Q H, Stekiel T A, Stadnicka A, Bosnjak Z J, Kampine J P
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Anesthesiology. 1995 Sep;83(3):604-10. doi: 10.1097/00000542-199509000-00020.
The mechanisms producing hemodynamic changes during epidural anesthesia are incompletely understood. The role of capacitance changes in the splanchnic venous bed can be clarified by comparing blocks of differing segmental distributions. Specifically, we speculated that blocks that include the innervation to the mesenteric circulation alter hemodynamics, sympathetic activity, and venous capacitance to a greater extent than blocks without blockade of sympathetic nerves to this critical vascular bed.
Rabbits were studied during alpha-chloralose anesthesia and mechanical ventilation. Sympathetic efferent nerve activity to the mesenteric vessels was measured by surgically placed electrodes, and mesenteric vein diameter was measured by videomicroscopy. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Responses were compared after administration of epidural lidocaine using a dose and catheter level that limited anesthetic to lumbar levels (lumbar group) or thoracic levels (thoracic group). In addition, hemodynamic responses were recorded after thoracolumbar block in animals receiving alpha-chloralose but breathing spontaneously (spontaneous ventilation group) and in awake animals (awake group).
Mean arterial pressure decreased 38.3 +/- 5.8% in the thoracic group but only 16.5 +/- 2.8 in the lumbar group. Sympathetic efferent nerve activity decreased in the thoracic group but increased in the lumbar group. An increase in vein diameter followed thoracic epidural anesthesia, but venoconstriction was observed after lumbar epidural block. The addition of intravenous sedation with alpha-chloralose did not increase the hypotensive effect of epidural anesthesia in this model.
Block of sympathetic fibers to the splanchnic circulation with thoracic epidural lidocaine produces mesenteric venodilatation that contributes to hypotension in rabbits. A lesser decrease in blood pressure follows blocks limited to lower segments, because baroreceptor stimulation produces increased splanchnic sympathetic activity and mesenteric venoconstriction. Responses in this model are comparable with and without general anesthesia and mechanical ventilation. To minimize hemodynamic consequences, epidural blockade should ideally be confined to the fewest necessary segments, avoiding splanchnic innervation if possible.
硬膜外麻醉期间产生血流动力学变化的机制尚未完全明确。通过比较不同节段分布的阻滞情况,可阐明内脏静脉床容量变化的作用。具体而言,我们推测,与未阻滞该关键血管床交感神经的阻滞相比,包含肠系膜循环神经支配的阻滞对血流动力学、交感神经活动及静脉容量的影响更大。
在α-氯醛糖麻醉和机械通气期间对家兔进行研究。通过手术放置电极测量肠系膜血管的交感传出神经活动,采用视频显微镜测量肠系膜静脉直径。通过动脉插管监测心率和平均动脉压。使用将麻醉限制在腰椎水平的剂量和导管位置(腰椎组)或胸椎水平的剂量和导管位置(胸椎组)给予硬膜外利多卡因后,比较各项反应。此外,记录接受α-氯醛糖但自主呼吸的动物(自主通气组)和清醒动物(清醒组)在胸腰段阻滞后的血流动力学反应。
胸椎组平均动脉压下降38.3±5.8%,而腰椎组仅下降16.5±2.8%。胸椎组交感传出神经活动下降,而腰椎组则增加。胸椎硬膜外麻醉后静脉直径增加,但腰椎硬膜外阻滞后观察到静脉收缩。在该模型中,添加α-氯醛糖静脉镇静并未增加硬膜外麻醉的降压效果。
胸椎硬膜外利多卡因阻滞内脏循环的交感纤维会导致肠系膜静脉扩张,从而导致家兔低血压。限于较低节段的阻滞导致的血压下降较小,因为压力感受器刺激会使内脏交感神经活动增加和肠系膜静脉收缩。该模型中有无全身麻醉和机械通气时的反应相当。为尽量减少血流动力学后果,硬膜外阻滞理想情况下应限于最少的必要节段,尽可能避免内脏神经支配。