摘要
目的 观察NO对岛状肌皮瓣I/R损伤的影响并探讨其作用机制。方法 选用白色小家猪 15只 ,随机分为I/R组、I/R +NO供体L -arg组及对照组。制作猪腹直肌岛状肌皮瓣I/R模型 ,于再灌注前后给予L -arg ,检测I/R不同时相皮瓣静脉血中NO的间接含量、皮瓣NTR渗出 ,计算再灌注完毕后肌肉存活比例。结果 ①I/R +L -arg组再灌注 0 .5小时、1小时NO间接含量 ( 75 .0 7± 12 .5 4 ) μmol/L、( 86.86± 2 0 .15 ) μmol/L ,明显高于I/R组 ( 4 6.75± 11.77) μmol/L、( 4 0 .3 8± 10 .78) μmol/L(P <0 .0 1)。②再灌注 1小时、4小时I/R +L -arg组皮瓣NTR计数 ( 66.5 0± 17.3 3~ 15 3 .80± 3 8.5 3 ) / 2 0个高倍视野明显低于I/R组 ( 171.5 0± 4 4 .5 0 ,3 16.80± 5 2 .85 ) / 2 0个高倍视野 (P <0 .0 1)。③再灌注完毕后 ,I/R +L -arg组皮瓣肌肉的存活比例 ( 83 .70± 15 .60 ) %明显高于I/R组 ( 2 4 .0 7± 12 .3 5 ) % (P <0 .0 1)。结论 于缺血后再灌注前及再灌注早期给予L -arg ,适当增加内源性NO的产生 ,能有效减轻肌皮瓣缺血再灌注损伤。
Objective To investigate the effects and mechanism of applying NO precursor L-arginine against ischemia and reperfusion injury of myocutaneous flap in pigs. Methods The epigastric myocutaneous island flaps models were set up. The flaps were divided into three groups: Ⅰ control group, Ⅱ ischemia-reperfusion group treated with saline, Ⅲ ischemia-reperfusion group treated with L-arginine. In groupⅡand Ⅲ, each flap was subjected to 6 hours of arterial-venous ischemia followed by 4 hours of perfusion. A bolus administration(30mg/kg) of L-arginine was given before the onset of reperfusion, followed by a continuous infusion of 10mg/(kg·min -1 ) for 1 hour. Serum NO contents, neutrophil counts, and muscle viability ratio in flap were determined. Results ①After 0.5 and 1 hour of reperfusion serum NO contents in group Ⅲ were significantly increased compared with group Ⅱ (P<0.01) and group Ⅰ (P<0.01). ②Neutrophil counts after 1 and 4 hours of reperfusion were significantly decreased in ischemia-reprefusion flaps treated with L-arginine as compared with group Ⅱ (P<0.01). ③Flap measurements revealed that the average area of muscle survival was 83.70±15.60 percent in group Ⅲ, which was significantly greater than that in group Ⅱ, in which only 24.07±12.35 percent of the muscle was viable (P<0.01). Conclusion These results demonstrate that administration of L-arginine before and during the initial hour of reperfusion signifcantly improves myocutaneous flap survival. The mechanism of action seems to be related to nitric oxide mediated suppression of ischemia-reperfusion injury through neutrophil activity inhibition.
出处
《实用美容整形外科杂志》
2002年第2期67-70,共4页
Journal of Practical Aesthetic and Plastic Surgery