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严重猪败血症中,血浆输注诱导补体激活相关的致命性心肌抑制和循环衰竭。

Fatal myocardial depression and circulatory collapse associated with complement activation induced by plasma infusion in severe porcine sepsis.

作者信息

Busund R, Balteskard L, Rønning G, Høgåsen K, Revhaug A

机构信息

Department of Surgery, Tromsø University Hospital, Norway.

出版信息

Acta Anaesthesiol Scand. 1995 Jan;39(1):100-8. doi: 10.1111/j.1399-6576.1995.tb05600.x.

DOI:10.1111/j.1399-6576.1995.tb05600.x
PMID:7725871
Abstract

We have previously reported that fresh frozen plasma (FFP) may induce a rapid irreversible shock when repeatedly infused in pigs challenged with Gram-negative sepsis. The aims of the present study were to elucidate the cardiovascular nature of the shock and determine the aetiologic role of tumour necrosis factor (TNF), complement activation and halothane anaesthesia. Three groups of anaesthetized piglets were inoculated with a lethal dose of live E. coli bacteria. Groups I (n = 8) and III (n = 8) were anaesthetized with halothane and group II (n = 8) with ketamine. Animals in groups I and II received repeated infusions of FFP, whereas animals in group III received repeated infusions of 7% albumin. Six animals in group I and four animals in group II died during the first plasma infusion. Survival time was significantly longer in group II (P = 0.04) compared to group I. No animals in group III died during the albumin infusions, and no adverse effects were observed during the infusions. In group I the plasma induced shock was characterized by abruptly falling mean arterial pressure, cardiac index, systemic vascular resistance index and left ventricular contractility. Concomitant increases were recorded in left ventricular filling pressure and central venous pressure. Group II demonstrated a similar, but delayed response. Plasma infusion was associated with a significant increase in terminal complement complex (TCC) (P < 0.03 in group I, P < 0.05 in group II) and depletion of serum ionized calcium. We conclude that FFP may induce fatal myocardial depression and circulatory collapse in severe sepsis. Complement activation may be of aetiologic importance.

摘要

我们之前曾报道,在受到革兰氏阴性菌败血症攻击的猪身上反复输注新鲜冷冻血浆(FFP)时,可能会引发快速且不可逆的休克。本研究的目的是阐明休克的心血管本质,并确定肿瘤坏死因子(TNF)、补体激活和氟烷麻醉的病因学作用。将三组麻醉仔猪接种致死剂量的活大肠杆菌。第一组(n = 8)和第三组(n = 8)用氟烷麻醉,第二组(n = 8)用氯胺酮麻醉。第一组和第二组的动物接受FFP的反复输注,而第三组的动物接受7%白蛋白的反复输注。第一组的6只动物和第二组的4只动物在首次输注血浆期间死亡。与第一组相比,第二组的存活时间显著更长(P = 0.04)。第三组在输注白蛋白期间没有动物死亡,且输注期间未观察到不良反应。在第一组中,血浆诱导的休克表现为平均动脉压、心脏指数、全身血管阻力指数和左心室收缩力突然下降。同时左心室充盈压和中心静脉压升高。第二组表现出类似但延迟的反应。血浆输注与终末补体复合物(TCC)显著增加相关(第一组P < 0.03,第二组P < 0.05)以及血清离子钙的消耗。我们得出结论,在严重败血症中,FFP可能会诱发致命的心肌抑制和循环衰竭。补体激活可能具有病因学重要性。

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