Bowers T K, Ozolins A L, Ratliff N B, Jacob H S, Hammerschmidt D E
Inflammation. 1983 Mar;7(1):1-13. doi: 10.1007/BF00918003.
We have postulated a role for activated plasma complement and for stimulated granulocytes in the triggering events of the adult respiratory distress syndrome (ARDS). Because brief periods of complement activation have proved to be pale mimics of the clinical syndrome, we extended our earlier models by infusing potently activated plasma complement into rabbits over a prolonged period of time (3 h). The expected leukostasis occurred, but pulmonary dysfunction remained modest. Nonetheless, piecemeal microvascular necrosis did develop, rendering this current model more credible than former models as a mimic of triggering events in ARDS; longer-term follow-up of such animals will be necessary to determine if this is indeed the case. Perhaps of even greater interest, the neutrophilic leukostasis was observed to progress over the 3 h to a predominantly lymphocytic leukostasis, a dramatically more rapid progression than is typical of such immune complex diseases as serum sickness and the Arthus reaction; further studies are in progress to elucidate the mechanism of this lymphostasis.
我们推测活化的血浆补体和受刺激的粒细胞在成人呼吸窘迫综合征(ARDS)的触发事件中起作用。由于短暂的补体激活已被证明只是该临床综合征的微弱模拟,我们通过在较长时间(3小时)内向兔子输注强效活化的血浆补体来扩展我们早期的模型。预期的白细胞淤滞出现了,但肺功能障碍仍然较轻。尽管如此,确实发生了散在的微血管坏死,使得这个当前模型作为ARDS触发事件的模拟比以前的模型更可信;有必要对这些动物进行长期随访以确定是否确实如此。也许更有趣的是,观察到中性粒细胞淤滞在3小时内进展为主要是淋巴细胞淤滞,这一进展速度比血清病和阿瑟斯反应等免疫复合物疾病的典型进展速度要快得多;正在进行进一步的研究以阐明这种淋巴细胞淤滞的机制。