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Fatal myocardial depression and circulatory collapse associated with complement activation induced by plasma infusion in severe porcine sepsis
Author(s) -
Busund R.,
Balteskard L.,
Rønning G.,
Høgåsen K.,
Revhaug A.
Publication year - 1995
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1995.tb05600.x
Subject(s) - medicine , shock (circulatory) , sepsis , anesthesia , circulatory collapse , cardiac index , circulatory system , septic shock , mean arterial pressure , central venous pressure , blood pressure , vascular resistance , halothane , contractility , albumin , hemodynamics , cardiac output , heart rate
Presented in part at the 34th World Congress of Surgery of the ISS/SIC and the 12th World Congress of the CICD, Stockholm, August 1991 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.