Becker G L, Pelligrino D A, Miletich D J, Albrecht R F
Anesth Analg. 1986 Apr;65(4):355-9.
The influence of N2O on O2 consumption by mitochondria isolated from the cerebral cortex of goats was examined in incubations preequilibrated with N2O-O2 or N2-O2. Rates of O2 consumption were measured polarographically in a closed system while adenosine triphosphate (ATP) formation was maximal (after addition of excess adenosine diphosphate (ADP), state 3 respiration) and then when it was at zero (after addition of excess oligomycin, state 4 respiration). Compared with 90% N2, 90% N2O produced no change in the rate of state 3 respiration; but an observed 9% decrease in the state 4 rate and an 11% increase in the state 3: state 4 ratio were statistically significant (P less than 0.05). These differences were not seen with N2 and N2O at 70% rather than at 90%, or when succinate rather than pyruvate-malate was used as the respiratory substrate. We conclude the following: Unlike other inhalation anesthetics, N2O at comparable anesthetic concentrations does not inhibit mitochondrial electron transport or ATP formation coupled to it (oxidative phosphorylation). N2O does inhibit one or more other processes, as yet unidentified, which are energetically coupled to electron transport. The increased cerebral O2 consumption that accompanies N2O anesthesia cannot be attributed to a direct effect of N2O on mitochondrial respiration.
在以N₂O - O₂或N₂ - O₂预平衡的孵育体系中，研究了N₂O对从山羊大脑皮层分离的线粒体耗氧量的影响。在封闭系统中用极谱法测量耗氧率，同时测定三磷酸腺苷（ATP）形成达到最大值时（加入过量二磷酸腺苷（ADP）后，状态3呼吸）以及ATP形成量为零时（加入过量寡霉素后，状态4呼吸）的耗氧率。与90% N₂相比，90% N₂O对状态3呼吸速率无影响；但观察到状态4速率下降9%，状态3与状态4的比率增加11%，这些差异具有统计学意义（P < 0.05）。当N₂和N₂O浓度为70%而非90%，或者使用琥珀酸而非丙酮酸 - 苹果酸作为呼吸底物时，未观察到这些差异。我们得出以下结论：与其他吸入麻醉剂不同，在可比的麻醉浓度下，N₂O不会抑制线粒体电子传递或与之偶联的ATP形成（氧化磷酸化）。N₂O确实会抑制一个或多个其他尚未明确的过程，这些过程在能量上与电子传递偶联。N₂O麻醉时伴随的大脑耗氧量增加不能归因于N₂O对线粒体呼吸的直接作用。
