Role of nitric oxide in iron-induced toxicity in rat hearts
- Author:
- No author available
- Journal Title:
- ACTA PHYSIOLOGICA SINICA
- Issue:
- 4
- DOI:
- 10.3321/j.issn:0371-0874.2002.04.005
- Key Word:
- 铁;心脏;一氧化氮;L-精氨酸;Nω-硝基-L-精氨酸甲酯
Abstract： 采用Langendorff灌流大鼠心脏和酶解分离的心肌细胞为实验模型, 研究铁负荷下心肌损伤情况以及一氧化氮(NO)在铁诱导的心肌损伤中的地位.结果显示: (1)心肌铁负荷(Fe-HQ)可使分离心肌细胞舒张期细胞长度缩短、收缩幅度和速度降低, 离体灌流心脏左室发展压(LVDP)、±dp/dtmax、冠脉流量呈现双相变化; 冠脉流出液中乳酸脱氢酶(LDH)、肌酸激酶(CK)释放量和心肌丙二醛(MDA)增高. (2)NO的前体L-精氨酸(L-arginine, L-Arg)引起心肌细胞舒张期细胞长度缩短、收缩幅度降低.离体灌流心脏LVDP、冠脉流量、和±dp/ dtmax增高, 用K-H液复灌后可恢复正常. (3)L-Arg预处理, 再行Fe-HQ灌流, 与单纯的L-Arg或Fe-HQ组相比, 心肌细胞舒张期细胞长度、收缩幅度和速度减小; 离体灌流心脏LVDP、±dp/ dtmax、心率和冠脉流量明显下降, 冠脉流出液中LDH、 CK增加. (4)Nω-硝基-L-精氨酸甲酯(L-NAME)和Fe-HQ合并灌流后, 与单纯Fe-HQ组相比, 心肌细胞舒张期细胞长度、收缩幅度和速度增加.L-NAME可阻断Fe-HQ引起的LVDP、左室舒张末压(LVEDP)和±dp/ dtmax降低, 冠脉流出液中LDH、 CK增高. (5)用Triton X-100短暂处理以去除冠脉内皮后, 与保留冠脉内皮的心肌相比, Fe-HQ引起的LVDP和±dp/ dtmax的一过性增高现象被抑制, 但对复灌期LVDP和±dp/ dtmax的改变无明显影响.上述实验结果表明, L-Arg可加重铁诱导的心肌损伤作用; L-NAME可通过抑制NOS减轻铁引起的心肌损伤, 其中冠脉内皮参与了铁的早期心肌作用.
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