摘要:
目的:观察亚牛磺酸对离体大鼠心肌缺血再灌注损伤的影响,探讨其保护的可能机制。方法:应用Langendorff恒压灌注大鼠心脏,停灌/复灌方式制备缺血再灌注模型。观察缺血/再灌注期间心脏收缩期左心室内压上升的最大变化速率(+LVdp/dtmax)、舒张期左心室内压下降的最大变化速率(-LVdp/dtmax)及左室发展压(LVDP)及心率(HR);采用比色法检测大鼠乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量的变化。结果:10-6、10-5 mol/L亚牛磺酸可以增加缺血/再灌注损伤后心脏±LVdp/dtmax、LVDP及HR (P<0.05~P<0.01),降低流出液中LDH水平(P<0.01),增加心肌组织中SOD活性(P<0.05~P<0.01),减少心肌组织中MDA的生成(P<0.01)。结论:亚牛磺酸可拮抗缺血/再灌注引起的心脏收缩及舒张功能障碍,其保护机制可能与增加心肌清除氧自由基的能力及改变心肌细胞膜稳定性有关。
Abstract:
Objective: To observe the influence of hypotaurine on ischemia/reperfusion injury(IRI) in isolated hearts in rats and to study its machanism.Methods: The ischemia/reperfusion(I/R) model of isolated perfused hearts was established by stopping and reperfusing Krebs-Henseleit(KH) fluid to the hearts of the rats.The changes of maximal rate of the pressure(+LVdp/dtmax) increase,maximal rate of the pressure(-LVdp/dtmax) decrease,left ventricular developed pressure(LVDP) of heart and heart rate(HR)were observed.Colorimetric method was used to assay the activity of lactate dehydrogenase(LDH),superoxide dismutase(SOD) and the content of malondialdehyde(MDA).Results: In the presence of 10-6 or 10-5 mol/L hypotaurine,±LVdp/dtmax was higher(P<0.05 or P<0.01),the leakage of mycardial LDH was attenuated(P<0.01),the SOD activity was increased(P<0.05 or P<0.01) and the content of MDA was decreased after reperfusion(P<0.01).Conclusions: Hypotaurine can prevent ischemia/reperfusion injury in isolated rat hearts,the mechanism of which may be related to its ability of clearing the oxygen-derived free radicals and stabilizing the cell membrane of the myocardium.
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