Saito T, Okazaki K, Sakata S, Tonogai S R, Tanaka Y, Takata K, Asai M, Matsuda F, Yamada Y, Tomino T, Tomino Y
Tohoku J Exp Med. 1977 Mar;121(3):289-99. doi: 10.1620/tjem.121.289.
Myocardial metabolism, blood flow distribution within the heart, and coronary and systemic circulations were observed during halothane anesthesia using 15 mongrel dogs. Pao2 and Paco2 were maintained near 100 and 40 torr respectively throughout the study. As arterial halothane content increased, most parameters of systemic circulation were depressed significantly. Coronary blood flow was reduced in parallel with myocardial oxygen consumption (MVo2) (r=+0.89, pless than0.001). Myocardial contractility decreased significantly as anesthesia deepened. MVo2 and myocardial CO2 production were reduced as arterial halothane concentration rose. Arterial-coronary venous difference in blood oxygen content remained unchanged even in deep stage. Lactate and pyruvate were continuously taken up by the myocardium, although the amounts of uptake were reduced as anesthesia progressed. Calculated excess lactate and redox potential did not show any signs of myocardial hypoxia even in deep halothane anesthesia. Among major hemodynamic parameters, left ventricular dp/dt max showed the closest correlation with MVo2. Microsphere injection method was used to observe blood flow distribution within the heart. Halothane did not influence the distribution significantly and I/O ratio of the left ventricular free wall remained near 1.0 during the study.
使用15只杂种狗,在氟烷麻醉期间观察心肌代谢、心脏内的血流分布以及冠状动脉和体循环。在整个研究过程中,动脉血氧分压(Pao2)和动脉血二氧化碳分压(Paco2)分别维持在接近100和40托。随着动脉血中氟烷含量增加,体循环的大多数参数显著降低。冠状动脉血流量与心肌耗氧量(MVo2)平行减少(r = +0.89,p <0.001)。随着麻醉加深,心肌收缩力显著下降。随着动脉血氟烷浓度升高,MVo2和心肌二氧化碳生成量减少。即使在麻醉深度期,动脉血与冠状动脉血的血氧含量差值仍保持不变。心肌持续摄取乳酸和丙酮酸,尽管随着麻醉进展摄取量减少。即使在深度氟烷麻醉下,计算得出的过量乳酸和氧化还原电位也未显示出任何心肌缺氧迹象。在主要血流动力学参数中,左心室dp/dt max与MVo2的相关性最为密切。采用微球注射法观察心脏内的血流分布。氟烷对分布没有显著影响,在研究期间左心室游离壁的输入/输出比保持在1.0左右。