ACTION OF HALOTHANE UPON MITOCHONDRIAL RESPIRATION
ACTION OF HALOTHANE UPON MITOCHONDRIAL RESPIRATION
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DOI：
10.1016/0003-9861(71)90507-8
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发表时间：
1971-01-01
影响因子：
3.9
通讯作者：
JENKINS, P
中科院分区：
文献类型：
--
作者：
HARRIS, RA;MUNROE, J;JENKINS, P
用大鼠肝线粒体(RLM3)、牛心线粒体(HBHM)和电子传递颗粒(ETP)研究了氟烷对呼吸的抑制作用。对于完整的线粒体准备，低浓度的氟烷(用气-液色谱测定~lt；2 MMA)显着抑制NADH连接底物的氧化，但不抑制琥珀酸氧化。氟烷的这种抑制作用是完全可逆的。相反，在较高浓度的麻醉剂下，许多其他线粒体过程被发现是不可逆的敏感方式。同样，HBHM、ETP和洗涤剂破坏的RLM对添加的NADH的氧化对低浓度的氟烷是可逆的。电子从琥珀酸到NAD的能量依赖性转移对氟烷也很敏感。而ETP的NADH-铁氰酸还原酶、琥珀酸氧化酶活性和微粒体的NADH-细胞色素还原酶活性均对氟烷不敏感。氟烷的抑制部位似乎在复合体I(NADH-CoQ还原酶)的鱼藤酮敏感部位附近。其他一些全身麻醉药在与氟烷相同的部位或附近抑制呼吸。
The inhibitory action of halothane upon respiration was studied with rat liver mitochondria (RLM3), beef heart mitochondria (HBHM), and electron-transport particles (ETP). With intact mitochondrial preparations the oxidation of NADH-linked substrates but not of succinate was markedly suppressed by low concentrations of halothane (<2 mmas determined by gas-liquid chromatography). This inhibitory action of halothane was completely reversible. In contrast, a number of other mitochondrial processes were found to be sensitive in an irreversible manner at higher concentrations of the anesthetic. Likewise, the oxidation of added NADH by HBHM, ETP, and detergent-disrupted RLM was found to be sensitive in a reversible manner to low concentrations of halothane. The energy-dependent transfer of electrons from succinate to NAD by ETPHwas also sensitive to halothane. On the other hand, the NADH-ferricyanide reductase and the succinic oxidase activities of ETP and the NADH-cytochromecreductase activity of microsomes were all insensitive to halothane. The site of inhibition by halothane appears to be in the vicinity of the rotenone-sensitive site of complex I (NADH-CoQ reductase). A number of other general anesthetics inhibited respiration at or near the same site as halothane.