Gardinali M, Tucci A, Bergamaschini L, Cicardi M
Boll Ist Sieroter Milan. 1982 Mar;61(1):1-7.
The C3a and C5a polypeptides release, under conditions of complement activation, causes a change in PMN shape and adhesiveness with formation of leukoemboli in microvascular districts. Those modified granulocytes produce oxygen radicals with toxic activity. This mechanism seems to play a role in different pathological situations like pulmonary distress in hemodialysis, leukapheresis, cardiopulmonary by-pass and extent of necrosis in acute myocardial infarction. The same mechanism has been largely investigated in Adult Respiratory Distress Syndrome (A.R.D.S.). In this condition the leukoembolization toxicity seems to be the most important pathogenetic factor of the alveolo-capillary membrane damage which is the base of the disease.
在补体激活的情况下，C3a和C5a多肽的释放会导致中性粒细胞形态和黏附性发生变化，并在微血管区域形成白细胞栓子。这些形态改变的粒细胞会产生具有毒性活性的氧自由基。这种机制似乎在不同的病理情况下发挥作用，如血液透析中的肺窘迫、白细胞分离术、体外循环以及急性心肌梗死中的坏死范围。同样的机制在成人呼吸窘迫综合征（A.R.D.S.）中也得到了大量研究。在这种情况下，白细胞栓塞毒性似乎是肺泡-毛细血管膜损伤的最重要致病因素，而这种损伤是该疾病的基础。
