Rowe G T, Eaton L R, Hess M L
J Mol Cell Cardiol. 1984 Nov;16(11):1075-9. doi: 10.1016/s0022-2828(84)80020-6.
Oxygen free radicals and their metabolites generated from activated neutrophils have been implicated in mediating the cardiovascular dysfunction of such diverse etiologies as myocardial ischemia and reperfusion injury, Gram negative sepsis, myocarditis and acute cardiac allograft rejection, but a direct demonstration of neutrophil derived oxygen free radical mediation of cardiovascular dysfunction has not been accomplished. In this study, we have demonstrated that activation of the canine neutrophil system, in vivo, results in the generation of oxygen free radicals that are capable of disrupting cardiovascular function producing a significant decrease in mean arterial pressure and cardiac index without any significant effect on the conduction system of the myocardium. Neutrophil depletion or pretreatment with superoxide dismutase and catalase inhibited the effects of activated neutrophils. This study provides evidence that neutrophil-derived reduced oxygen intermediates are able to induce severe cardiovascular dysfunction.
活化的中性粒细胞产生的氧自由基及其代谢产物被认为与多种病因引起的心血管功能障碍有关，如心肌缺血和再灌注损伤、革兰氏阴性菌败血症、心肌炎和急性心脏移植排斥反应，但尚未直接证明中性粒细胞衍生的氧自由基介导了心血管功能障碍。在本研究中，我们已经证明，犬中性粒细胞系统在体内的激活会导致氧自由基的产生，这些氧自由基能够破坏心血管功能，使平均动脉压和心脏指数显著降低，而对心肌传导系统没有任何显著影响。中性粒细胞耗竭或用超氧化物歧化酶和过氧化氢酶预处理可抑制活化中性粒细胞的作用。本研究提供了证据，表明中性粒细胞衍生的还原型氧中间体能够诱导严重的心血管功能障碍。
