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目的:一氧化氮(nitric oxide,NO)作为体内的一种细胞信使分子,在心血管活动中起重要作用。NO水平及其在体内的合成代谢通路与临床麻醉、危重症、术后恢复等密切相关。本实验通过使用H2O2在体外诱导人红细胞氧化应激反应,观察红细胞NO,eNOS,NO3-和NO2-水平的变化,及丙泊酚对这一变化的影响。方法:健康成年人红细胞制成2%红细胞悬液,分为10组:对照组(C组)、H2O2组(H组)、丙泊酚12.5μmol/L组,丙泊酚25μmol/L组,丙泊酚50μmol/L组,丙泊酚100μmol/L组,丙泊酚12.5μmol/L+H2O2组(P12.5+H组)、丙泊酚25μmol/L+H2O2组(P25+H组)、丙泊酚50μmol/L+H2O2组(P50+H组),丙泊酚100μmol/L+H2O2组(P100+H组)。各组H2O2的反应浓度均为200μmol/L,孵育30 min,测定红细胞NO,eNOS,NO3-和NO2-水平的变化。结果:P50组(4.97±0.58)NO水平高于其余各组(P<0.05);H组(4.96±0.52)NO水平高于其它组(P<0.05);与C组(1.34±0.29)相比,P50组(2.23±0.33)和H组(2.33±0.39)eNOS水平升高(P<0.05);NO3-水平H组(43.78±2.13)比C组(52.06±2.14)低(P=0.017);NO2-水平H组(13.32±2.04)比C组(34.14±1.48)低(P=0.025)。结论:丙泊酚和H2O2能够使红细胞NO和eNOS水平的升高;H2O2引起红细胞NO升高和NO3-,NO2-的降低。我们推断,H2O2使体内产生的过量NO,会对机体产生害影响,而丙泊酚通过清除自由基、抑制H2O2诱导的红细胞硝酸盐-亚硝酸盐-一氧化氮通路向氧化相移动来维持NO水平,实现维持NO生物利用率及保护人红细胞抵抗氧化损伤。
AIM: Nitric oxide (NO), as a cellular messenger molecule in the body, plays an important role in cardiovascular activity. The level of NO and its anabolic pathway in the body are closely related to clinical anesthesia, critically ill patients and postoperative recovery. In this experiment, the oxidative stress induced by human erythrocytes was induced by H2O2 in vitro to observe the change of NO, eNOS, NO3- and NO2- in erythrocytes and the effect of propofol on this change. METHODS: Healthy adult erythrocytes were made into 2% erythrocyte suspension and divided into 10 groups: control group (C group), H2O2 group (H group), propofol 12.5μmol / L group, propofol 25μmol / L group Propofol 50μmol / L group, Propofol 100μmol / L group, Propofol 12.5μmol / L + H2O2 group (P12.5 + H group), Propofol 25μmol / L + H2O2 group (P25 + H group) , 50μmol / L propofol + H2O2 group (P50 + H group) and 100μmol / L propofol + H2O2 group (P100 + H group). The reaction concentration of H2O2 in each group was 200μmol / L and incubated for 30 min. The changes of NO, eNOS, NO3- and NO2- in erythrocytes were measured. Results: The levels of NO in the P50 group (4.97 ± 0.58) were higher than those in the other groups (P <0.05). The levels of NO in the H group (4.96 ± 0.52) were significantly higher than those in the other groups (P <0.05) (P <0.05); NO3-level H group (43.78 ± 2.13) was lower than that of C group (52.06 ± 2.14) (P = 0.017), P50 group (2.23 ± 0.33) and H group ); NO2-level H group (13.32 ± 2.04) was lower than C group (34.14 ± 1.48) (P = 0.025). CONCLUSION: Propofol and H2O2 can increase the levels of NO and eNOS in erythrocytes. H2O2 causes elevated levels of NO in erythrocytes and decreases in NO3- and NO2-. We conclude that excessive NO generated by H2O2 will have a harmful effect on the body, while propofol inhibits NO by scavenging free radicals and inhibiting H2O2-induced red cell nitrite-nitrite-nitric oxide pathway from moving toward the oxidized phase Level to achieve the maintenance of NO bioavailability and protect human erythrocytes against oxidative damage.