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. 1996 Feb;82(2):349-57. doi: 10.1097/00000539-199602000-00024.
The purpose of the present study was to quantify the inhibitory effect of inhaled halothane and isoflurane on acute hypercapnia-induced responses of capacitance-regulating veins and related cardiovascular variables in response to sequential 40-s periods of 5%, 10%, 15%, and 20% inspired CO2 (FICO2). Measurements were made in normoxic alpha-chloralose-anesthetized rabbits before, during, and after either 0.75 minimum alveolar anesthetic concentration inhaled halothane or isoflurane. The graded hypercapnia caused graded venoconstriction and bradycardia but minimal pressor responses. Hypercapnia-induced venoconstriction was blocked by prior local superfusion of the exposed veins with 3 x 10(-6) M tetrodotoxin. Both the hypercapnia-induced venoconstriction and bradycardia responses were significantly attenuated by halothane or isoflurane and did not fully recover after removal of the anesthetics from the circulation. Both anesthetics produced a significant baseline (i.e., prehypercapnia) hypotension and a tendency toward a resultant tachycardia. The baseline hypotension did not recover completely after elimination of the anesthetic. Neither anesthetic altered baseline vein diameter. These results agree with previous studies demonstrating that hypercapnic acidosis produces mesenteric venoconstriction by elevating excitatory sympathetic efferent neural input via activation of peripheral and central chemoreceptors and that bradycardia results from activation of compensatory baroreflexes. The neural components of these reflexes are possible primary sites for attenuation of these cardiovascular responses by halothane and isoflurane.
本研究的目的是量化吸入氟烷和异氟烷对急性高碳酸血症诱导的容量调节静脉反应以及相关心血管变量的抑制作用，这些反应是对5%、10%、15%和20%吸入二氧化碳（FICO2）连续40秒时段的反应。在常氧α-氯醛糖麻醉的兔中，于吸入0.75最低肺泡麻醉浓度的氟烷或异氟烷之前、期间和之后进行测量。分级高碳酸血症引起分级静脉收缩和心动过缓，但升压反应极小。高碳酸血症诱导的静脉收缩可被预先用3×10⁻⁶ M河豚毒素对暴露静脉进行局部灌注所阻断。氟烷或异氟烷均显著减弱高碳酸血症诱导的静脉收缩和心动过缓反应，且在从循环中去除麻醉剂后未完全恢复。两种麻醉剂均产生显著的基线（即高碳酸血症前）低血压以及随之而来的心动过速倾向。消除麻醉剂后，基线低血压未完全恢复。两种麻醉剂均未改变基线静脉直径。这些结果与先前的研究一致，先前研究表明高碳酸性酸中毒通过激活外周和中枢化学感受器增加兴奋性交感传出神经输入来产生肠系膜静脉收缩，且心动过缓是由代偿性压力反射激活所致。这些反射的神经成分可能是氟烷和异氟烷减弱这些心血管反应的主要部位。
