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目的:观察N-正丁基氟哌啶醇碘化物(F_2)对大鼠心肌缺血再灌注损伤及大鼠心室肌细胞L-型钙电流(I_(Ca))的影响。方法:大鼠冠脉左前降支结扎30 min后恢复灌注30 min,于缺血前分别静脉注射F_2(1,2,和4 mg/kg)。测定血浆CK、CK-MB、LDH、HBDH、GOT、MDA的含量及SOD活性;观察心肌的形态学改变。采用酶急性分离的大鼠单个心室肌细胞,应用膜片箝全细胞记录技术,观察F_2对I_(Ca)的影响。结果:F_2呈量效依赖地降低缺血再灌注心肌酶CK、CK-MB、LDH、HBDH、GOT的释放,保护SOD的活性,降低MDA的产生;电镜下可见F_2减轻心肌的形态学改变。F_2 1 μmol/L明显抑制I_(Ca),使峰电流从(1775±360)pA减少至(464±129)pA(n=8,P<0.01),并使得I_(Ca)的I-V曲线上移,但不改变其电压依赖特征。结论:F_2对大鼠心肌缺血再灌注损伤具有拮抗作用,并可抑制大鼠心室肌细胞L-型钙电流。F_2对心肌缺血再灌注损伤的拮抗作用及其扩张血管的机制可能与其阻断L-型钙通道有关。
Objective: To observe the effect of Nn-butyl haloperidol iodide (F_2) on myocardial ischemia-reperfusion injury and L-type calcium current (I_ (Ca)) in rat ventricular myocytes. Methods: The left anterior descending coronary artery was ligated for 30 min and then reperfused for 30 min. F_2 (1, 2, and 4 mg / kg) were injected intravenously before ischemia. The content of CK, CK-MB, LDH, HBDH, GOT, MDA and the activity of SOD were measured. The morphological changes of myocardium were observed. The rat ventricular myocytes isolated from acute ventricular myocytes were harvested and patch clamp whole cell recording was used to observe the effect of F_2 on I_ (Ca). Results: F 2 dose-dependently reduced the release of myocardial CK, CK-MB, LDH, HBDH and GOT in ischemia-reperfusion rats, and protected the activity of SOD and decreased the production of MDA. F 2 reduced the morphological changes of myocardium. F_2 1 μmol / L significantly inhibited I_ (Ca) and decreased peak current from (1775 ± 360) pA to (464 ± 129) pA (n = 8, P <0.01) Moving, but not changing its voltage-dependent characteristics. Conclusion: F 2 can antagonize myocardial ischemia-reperfusion injury and inhibit L-type calcium current in rat ventricular myocytes. Antagonism of F 2 on myocardial ischemia-reperfusion injury and the mechanism of its dilatation of blood vessels may be related to its blocking of L-type calcium channel.