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硬膜外麻醉对内脏容量血管的影响。

Effects of epidural anesthesia on splanchnic capacitance.

作者信息

Hogan Q H, Stadnicka A, Kampine J P

机构信息

Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.

出版信息

Adv Pharmacol. 1994;31:471-83. doi: 10.1016/s1054-3589(08)60636-5.

Abstract

Splanchnic veins play an important role in the active control of total body circulatory capacitance. The effects of epidural anesthesia on splanchnic venous capacitance have not previously been examined. A rabbit model using direct measures of mesenteric vein diameter and sympathetic efferent nerve activity was used to test the response to epidural lidocaine at three different doses and to intramuscular lidocaine at two doses. Epidural anesthesia produced hypotension, mesenteric venodilatation, and interruption of sympathetic activity. Maximal changes of these parameters were comparable in the three epidural dosage groups but were more prolonged with increasing dose. High-dose systemic lidocaine caused smaller changes in arterial pressure and sympathetic activity. Further experiments were done to investigate the mechanism of splanchnic venodilatation. Passive vein distension and effects of circulating lidocaine or catecholamines are not likely contributing factors. Blocks limited to thoracic segments, but including the origin of splanchnic preganglionic fibers, produce comparable mesenteric venodilatation and sympathetic interruption as extensive thoracolumbar blocks. Blocks limited to lumbar segments, however, showed mesenteric venoconstriction and increased splanchnic sympathetic activity. The variable responses in splanchnic capacitance with the onset of epidural anesthesia are the result of the competing influences of increased sympathetic activity from decreasing blood pressure and blockade of sympathetic fibers to the splanchnic veins.

摘要

内脏静脉在全身循环容量的主动控制中发挥着重要作用。硬膜外麻醉对内脏静脉容量的影响此前尚未得到研究。采用直接测量肠系膜静脉直径和交感传出神经活动的兔模型,测试了三种不同剂量的硬膜外利多卡因和两种剂量的肌肉注射利多卡因的反应。硬膜外麻醉导致低血压、肠系膜静脉扩张和交感神经活动中断。这三个硬膜外剂量组中这些参数的最大变化相当,但随着剂量增加而持续时间更长。高剂量全身利多卡因引起的动脉压和交感神经活动变化较小。进一步的实验旨在研究内脏静脉扩张的机制。被动静脉扩张以及循环利多卡因或儿茶酚胺的作用不太可能是促成因素。仅限于胸段但包括内脏节前纤维起始部位的阻滞,产生的肠系膜静脉扩张和交感神经中断与广泛的胸腰段阻滞相当。然而,仅限于腰段的阻滞显示肠系膜静脉收缩和内脏交感神经活动增加。硬膜外麻醉开始时内脏容量的不同反应是血压下降导致交感神经活动增加与内脏静脉交感神经纤维阻滞相互竞争的结果。

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