Kearns S R, Kelly C J, Barry M, Abdih H, Condron C, Leahy A, Bouchier-Hayes D
Department of Surgery, Royal College of Surgeons in Ireland, Beaumont Hospital, Beaumont Road, Dublin 9, Ireland.
Eur J Vasc Endovasc Surg. 1999 Jun;17(6):533-6. doi: 10.1053/ejvs.1999.0833.
to evaluate vitamin C supplementation in the prevention of ischaemia-reperfusion (I-R) induced acute lung injury.
Sprague-Dawley rats (n =6/group) were randomised into Control, I-R and I-R pretreated with vitamin C (3.3 g over 5 days). Ischaemia-reperfusion injury was induced by 30 minutes infrarenal aortic cross-clamping and 120 minutes reperfusion.
pulmonary microvascular injury was measured by broncho-alveolar lavage protein concentration, pulmonary neutrophil infiltration by tissue myeloperoxidase activity and bronchoalveolar lavage neutrophil counts. In a second experiment (n =5/group) neutrophil respiratory burst activity was measured in Control and vitamin C groups.
ischaemia-reperfusion resulted in a significant increase in both microvascular leakage and pulmonary neutrophil infiltration as measured by bronchoalveolar lavage protein concentration and pulmonary myeloperoxidase activity respectively. Pretreatment with vitamin C significantly attenuated both microvascular leakage and neutrophil infiltration. Neutrophil respiratory burst activity was significantly reduced in the vitamin C group (13.02 m.c.f.+/-0.3) compared with Control (19.04 m.c.f.+/-1. 9),p <0.02.
these data suggest that oral vitamin C therapy protects against ischaemia-reperfusion-induced acute lung injury, possibly by attenuating neutrophil respiratory burst activity.
评估补充维生素C对预防缺血再灌注(I-R)诱导的急性肺损伤的作用。
将Sprague-Dawley大鼠(每组n = 6)随机分为对照组、I-R组和维生素C预处理的I-R组(5天内给予3.3 g维生素C)。通过肾下腹主动脉夹闭30分钟和再灌注120分钟诱导缺血再灌注损伤。
通过支气管肺泡灌洗蛋白浓度测量肺微血管损伤,通过组织髓过氧化物酶活性和支气管肺泡灌洗中性粒细胞计数测量肺中性粒细胞浸润。在第二个实验中(每组n = 5),测量对照组和维生素C组中性粒细胞呼吸爆发活性。
缺血再灌注分别导致支气管肺泡灌洗蛋白浓度和肺髓过氧化物酶活性测量的微血管渗漏和肺中性粒细胞浸润显著增加。维生素C预处理显著减轻了微血管渗漏和中性粒细胞浸润。与对照组(19.04 m.c.f.±1.9)相比,维生素C组中性粒细胞呼吸爆发活性显著降低(13.02 m.c.f.±0.3),p<0.02。
这些数据表明,口服维生素C疗法可预防缺血再灌注诱导的急性肺损伤,可能是通过减弱中性粒细胞呼吸爆发活性实现的。