Stekiel T A, Stekiel W J, Tominaga M, Stadnicka A, Bosnjak Z J, Kampine J P
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Anesth Analg. 1995 May;80(5):994-1001. doi: 10.1097/00000539-199505000-00025.
We measured the effects of inhaled isoflurane on hypoxemia-induced changes in the diameter of small mesenteric (capacitance-regulating) veins, sympathetic efferent neural activity, heart rate, and arterial blood pressure. Simultaneous changes in these dependent variables were measured in situ in response to 40-s periods of sequentially administered 10%, 5%, 2.5%, and 0% inspired oxygen before, during, and after either 0.75% or 1.5% vol/vol inhaled isoflurane in alpha-chloralose-anesthetized rabbits. Isoflurane inhibited hypoxia-mediated venoconstriction, increases in sympathetic efferent nerve activity, arterial hypertension, and bradycardia. Furthermore, inhibition of diameter, blood pressure, and heart rate responses persisted after washout of isoflurane. Differences in the attenuation of these respective hypoxia-mediated responses were minimal between the two concentrations of inhaled isoflurane. These results further demonstrate that isoflurane alters the ability to produce cardiovascular adjustments to circulatory stress, including changes in vascular capacitance, which is a major regulatory mechanism.
我们测量了吸入异氟烷对低氧血症引起的肠系膜小静脉（容量调节）直径变化、交感传出神经活动、心率和动脉血压的影响。在α-氯醛糖麻醉的兔中，于吸入0.75%或1.5%体积分数/体积的异氟烷之前、期间和之后，依次给予10%、5%、2.5%和0%的吸入氧40秒，同时原位测量这些因变量的变化。异氟烷抑制了缺氧介导的静脉收缩、交感传出神经活动增加、动脉高血压和心动过缓。此外，异氟烷洗脱后，直径、血压和心率反应的抑制仍持续存在。两种吸入异氟烷浓度之间，这些各自缺氧介导反应的衰减差异极小。这些结果进一步证明，异氟烷改变了对循环应激产生心血管调节的能力，包括血管容量的变化，这是一种主要的调节机制。
