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目的 明确一氧化氮 (NO)是否诱导预处理心肌细胞早期保护作用。方法 取体外培养的新生大鼠心肌细胞 ,分为如下各组 :①阴性对照组 (Normal组 ) ;②SNAP(5 0 0 μmol·L-1)预处理组 (NO组 ) ;③缺氧预处理组 (HP组 ) ;④NO合成抑制剂L NAME作用细胞后再行缺氧预处理组 (L NAME +HP组 ) ;⑤L 精氨酸 (L Arg)预处理心肌细胞组(L Arg组 ) ;⑥L NAME与L Arg共同作用于心肌细胞组(L NAME +L Arg组 ) ;⑦缺氧复氧损伤组 (H/R组 )。②～⑥组细胞在给予干预因素后使细胞经历 6h缺氧及 3h复氧 ,阳性对照组不予任何处理直接使其缺氧 6h复氧 3h。分别检测心肌细胞存活率及乳酸脱氢酶 (LDH)活性 ,以判定心肌细胞损伤程度。结果 NO预处理心肌细胞后使其缺氧复氧损伤减轻 ,表现为与单纯缺氧复氧组细胞比较其培养上清LDH活性降低 ,细胞存活率提高 (P <0 0 1) ;缺氧预处理和L Arg预处理细胞均可减轻心肌细胞缺氧复氧损伤 (P<0 0 1) ,但此作用可被NOS抑制剂L NAME所拮抗。结论 内源性及外源性NO均可诱导心肌细胞预处理早期保护作用
Objective To determine whether nitric oxide (NO) induces early protection of cardiomyocytes. Methods The neonatal rat cardiomyocytes cultured in vitro were divided into the following groups: ① negative control group (Normal group); ② SNAP (500 μmol·L-1) pretreatment group (NO group); ③ hypoxic preconditioning Group (HP group); ④NOS inhibitor L NAME-treated cells followed by hypoxic preconditioning group (L NAME + HP group); ⑤ L Arg preconditioning group (L Arg group); ⑥L NAME and L Arg act in cardiomyocytes group (L NAME + L Arg group); ⑦ Hypoxia and reoxygenation injury group (H / R group). ② ~ ⑥ group of cells given intervention after the cells underwent 6h hypoxia and 3h reoxygenation, positive control without any treatment directly to hypoxia 6h reoxygenation 3h. The survival rate of cardiomyocytes and the activity of lactate dehydrogenase (LDH) were detected to determine the extent of cardiomyocyte injury. Results NO pretreatment of cardiomyocytes reduced the hypoxia-reoxygenation injury. The results showed that compared with hypoxia-reoxygenation group, the activity of LDH decreased and the cell survival rate increased (P <0.01) Both L-Arg and L-Arg preconditioned cells could reduce cardiomyocytes hypoxia-reoxygenation injury (P <0.01), but this effect could be antagonized by NOS inhibitor L NAME. Conclusion Both endogenous and exogenous NO can induce the early protective effect of cardiomyocytes preconditioning