Runzer Tim D, Ansley David M, Godin David V, Chambers Gordon K
Department of Anesthesia, University of British Columbia, Canada.
Anesth Analg. 2002 Jan;94(1):89-93, table of contents. doi: 10.1097/00000539-200201000-00017.
The effects of anesthesia on ischemia-reperfusion injury are of considerable scientific and clinical interest. We examined the effects of propofol (known to possess antioxidant activity) and halothane (devoid of antioxidant activity in vitro) on tissue and red blood cell (RBC) antioxidant capacity. Adult male Wistar rats were anesthetized with halothane 0.5%-1.0% (n = 7), propofol 500 microg x kg(-1) x min(-1) with halothane 0.25%-0.5% (small-dose propofol; n = 9), or propofol 2000 microg x kg(-1) x min(-1) (large-dose propofol; n = 8) for 45 min. Blood and tissue samples of liver, kidney, heart, and lung were then harvested for in vitro exposure to a peroxidizing agent. Red cell malondialdehyde and tissue thiobarbituric acid reactive substances were determined spectrophotometrically. Antioxidant capacities of blood and tissues in the Large-Dose Propofol group, and of blood and all tissues except lung in the Small-Dose Propofol group, were increased significantly compared with halothane (P < 0.003). The increases in tissue antioxidant capacities varied in their magnitude: RBC > liver > kidney > heart > lung. There was a high correlation between changes in RBC susceptibility to oxidative damage and corresponding changes in tissues. These findings demonstrate that large-dose propofol significantly enhances tissue antioxidant capacity, and RBC antioxidant capacity can serve as a functional measure of tissue activity, in vivo.
We designed this study to investigate the antioxidant effects of propofol in various tissues in a rat model. Pretreatment of animals with propofol led to a reduction in the susceptibility to an in vitro oxidative stress of five different tissues investigated, demonstrating the drug's ability to limit oxidative injury. This may have future application in limiting organ dysfunction after periods of tissue ischemia (which results in oxidative damage).
麻醉对缺血再灌注损伤的影响具有重大的科学和临床意义。我们研究了丙泊酚(已知具有抗氧化活性)和氟烷(在体外缺乏抗氧化活性)对组织和红细胞(RBC)抗氧化能力的影响。成年雄性Wistar大鼠分别用0.5%-1.0%氟烷(n = 7)、丙泊酚500μg·kg⁻¹·min⁻¹加0.25%-0.5%氟烷(小剂量丙泊酚;n = 9)或丙泊酚2000μg·kg⁻¹·min⁻¹(大剂量丙泊酚;n = 8)麻醉45分钟。然后采集血液以及肝、肾、心和肺的组织样本,用于体外暴露于过氧化剂。通过分光光度法测定红细胞丙二醛和组织硫代巴比妥酸反应性物质。与氟烷组相比,大剂量丙泊酚组血液和组织以及小剂量丙泊酚组血液和除肺以外的所有组织的抗氧化能力显著增加(P < 0.003)。组织抗氧化能力的增加幅度各不相同:RBC>肝>肾>心>肺。RBC对氧化损伤易感性的变化与组织中的相应变化高度相关。这些发现表明,大剂量丙泊酚可显著增强组织抗氧化能力,且RBC抗氧化能力可作为体内组织活性的功能性指标。
我们设计本研究以探讨丙泊酚在大鼠模型中对各种组织的抗氧化作用。用丙泊酚预处理动物可降低所研究的五种不同组织对体外氧化应激的易感性,证明了该药物限制氧化损伤的能力。这可能在限制组织缺血(导致氧化损伤)后的器官功能障碍方面具有未来应用价值。