| Autor: |
Nonami, Yoshiki, Rao, Vivek, Shiono, Noritsugu, Ogoshi, Shohei |
| Zdroj: |
Surgery Today; April 1998, Vol. 28 Issue: 4 p379-384, 6p |
| Abstrakt: |
Abstract: Neutrophil activation and oxygen-derived free radical formation have been implicated in cardiac ischemiareperfusion injury. To elucidate the mechanism of ischemiareperfusion injury, we thus determined the effect of the nitric oxide (NO) precursorl-arginine on the free radical injury of cultured cardiomyocytes which were obtained from patients undergoing corrective surgery for tetralogy of Fallot. Free radicals were generated from hypoxanthine via xanthine oxidase, and the cellular changes were determined microscopically. All concentrations of L-arginine (0.5 to 3 mM) prolonged the myocyte survival time compared to the control group, with 0.5 mMl-arginine increasing the survival time to the greatest extent. Cellular susceptibility to free radical injury was the lowest with 0.5 mMl-arginine. Further experiments were performed with 0.5 mMl-arginine plus 100 mM or 1 000 mM of the NO synthase (NOS) inhibitorN G -nitro-l-arginine methylester (l-NAME) to determine whether or not the effects of L-arginine are mediated through the NO pathway. The survival time for the cells treated with a concentration ofl-NAME was shorter than for the cells treated with 0.5 mMl-arginine alone. These results suggest thatl-arginine acts through the NO-dependent pathway. In conclusion, our findings thus confirmed the quenching effects of NO on free radical injury in cultured cardiomyocytes. |
| Databáze: |
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