Complement activation, @entity2232 and XXXX in relation to the cardiovascular response to endotoxin-induced systemic @entity32 in healthy volunteers.

@entity1 @entity32 @entity295 @entity5694 @entity2232 @entity7766 @entity3162 @entity26 @entity842 @entity526
BACKGROUND: Endotoxin is a major stimulus for triggering the host response in @entity295 . The pathophysiology of @entity295 involves activation of the vascular endothelium and leukocytes, resulting in the release of various mediators, e.g. cytokines, @entity842 (NO), endothelin (ET-1) and complement factors. We evaluated the blood levels of complement activation, ET-1 and @entity7766 (NPY) in parallel with the haemodynamic and @entity26 transport response during @entity1 experimental @entity5694 . METHODS: Eleven healthy @entity1 had venous, arterial and pulmonary arterial catheters placed for continuous haemodynamic measuring. After 30 min rest endotoxin ( @entity526 4 ng kg(-1), Lot G1) was intravenously administered. Blood samples from pulmonary and arterial catheters were collected hourly over 4 h. RESULTS: Body temperature augmented significantly from baseline values (36.7 +/- 0.7 degrees C, mean +/- SEM) with a maximum after 3.5 h (39.1 +/- 0.3 degrees C, P < 0.001). Cardiac output increased by 100%, systemic vascular resistance decreased by 50%, the @entity26 consumption and the tissue @entity26 transport increased. Activation of the complement system was indicated by an increase in SC5b-9. @entity2232 -like immunoreactivity (ET-1- @entity3162 ) increased over time in arterial blood. NPY-like immunoreactivity (NPY- @entity3162 ) did not change over time. CONCLUSION: A dose of endotoxin associated with reproducible systemic vasodilation and fever in healthy subjects causes complement activation and increased systemic levels of ET-1- @entity3162 , illustrating that the model is a useful tool for inducing moderate systemic @entity32 where several mediator systems are activated.
