McCallum J B, Stekiel T A, Bosnjak Z J, Kampine J P
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
Anesth Analg. 1993 May;76(5):1095-105. doi: 10.1213/00000539-199305000-00032.
Volatile anesthetics act at a number of sites to alter cardiovascular function and the response of the cardiovascular system to barostatic reflexes. We examined the effects of isoflurane on reflex regulation of mesenteric venous capacitance vessels. To determine whether isoflurane alters mesenteric venous capacitance, continuous direct observations of mesenteric vein diameter, intravenous pressure, and mesenteric sympathetic efferent nerve activity (SENA) were made in 31 chloralose-anesthetized New Zealand white rabbits. Simultaneous measurements were obtained for aortic pressure and heart rate. The responses to changes in baroreceptor activation by means of either bilateral carotid occlusion (BCO) or aortic nerve stimulation (ANS) were studied in one group of 18 rabbits, while the response to direct electric activation by means of celiac ganglion stimulation (CGS) was studied in another group of 13 rabbits. In both groups, isoflurane vapor was administered at levels of 0.75% or 1.5%, and superfused isoflurane was administered directly to the vessel in doses of either 3% or 5% equilibrated with physiologic salt solution. Anesthetic levels were verified by mass spectrometry for expired gas and by gas chromatography for blood and superfusate levels. Inhaled isoflurane reduced hemodynamic variables and SENA in a dose-dependent fashion, but these same variables were unaffected by superfused isoflurane. One and one-half percent inhaled isoflurane abolished all reflex responses to baroreceptor stimulation in mesenteric capacitance veins and in SENA, but superfused isoflurane produced no corresponding attenuation of reflex responses to baroreceptor stimulation. Neither inhaled nor superfused isoflurane suppressed the reflex venoconstriction in response to CGS. Both inhaled and superfused isoflurane dilated the baseline vein diameter before stimulation. These results indicate that isoflurane dose increase the diameter of mesenteric venous capacitance vessels and inhibits reflex-induced constriction of mesenteric veins, whereas mesenteric sympathetic efferent nerve activity decreases and the reflex responses to activation of the carotid sinus and aortic baroreceptors are attenuated by inhaled isoflurane. The mechanism of this action appears to be primarily through the inhibition of central or peripheral sympathetic ganglionic transmission of barostatic control.
挥发性麻醉药作用于多个部位，以改变心血管功能以及心血管系统对压力反射的反应。我们研究了异氟烷对肠系膜静脉容量血管反射调节的影响。为了确定异氟烷是否改变肠系膜静脉容量，我们对31只氯醛糖麻醉的新西兰白兔进行了肠系膜静脉直径、静脉压和肠系膜交感传出神经活动（SENA）的连续直接观察。同时测量主动脉压和心率。在一组18只兔子中研究了通过双侧颈动脉闭塞（BCO）或主动脉神经刺激（ANS）改变压力感受器激活的反应，而在另一组13只兔子中研究了通过腹腔神经节刺激（CGS）进行直接电激活的反应。在两组中，均以0.75%或1.5%的浓度给予异氟烷蒸气，并以3%或5%的剂量将与生理盐溶液平衡的异氟烷直接灌注到血管中。通过质谱法检测呼出气体中的麻醉水平，并通过气相色谱法检测血液和灌注液中的麻醉水平。吸入的异氟烷以剂量依赖的方式降低血流动力学变量和SENA，但这些相同的变量不受灌注异氟烷的影响。1.5%的吸入异氟烷消除了肠系膜容量静脉和SENA对压力感受器刺激的所有反射反应，但灌注异氟烷对压力感受器刺激的反射反应没有相应的减弱。吸入和灌注的异氟烷均未抑制对CGS的反射性静脉收缩。吸入和灌注的异氟烷在刺激前均使基线静脉直径扩张。这些结果表明，异氟烷剂量增加会使肠系膜静脉容量血管的直径增大，并抑制反射性引起的肠系膜静脉收缩，而肠系膜交感传出神经活动减少，吸入异氟烷会减弱对颈动脉窦和主动脉压力感受器激活的反射反应。这种作用机制似乎主要是通过抑制压力控制的中枢或外周交感神经节传递。
