Complement activation, endothelin-1 and neuropeptide Y in relation to the cardiovascular response to endotoxin-induced systemic inflammation in healthy volunteers.

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Soop, A (author)

Complement activation, endothelin-1 and neuropeptide Y in relation to the cardiovascular response to endotoxin-induced systemic inflammation in healthy volunteers.

Article/chapterEnglish2004

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Wiley,2004

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LIBRIS-ID:oai:gup.ub.gu.se/62938
https://gup.ub.gu.se/publication/62938URI
http://kipublications.ki.se/Default.aspx?queryparsed=id:1930393URI
https://doi.org/10.1111/j.1399-6576.2004.00273.xDOI

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Language:English

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SwePubSwePub

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Subject category:ref swepub-contenttype
Subject category:art swepub-publicationtype

Notes

BACKGROUND: Endotoxin is a major stimulus for triggering the host response in septicaemia. The pathophysiology of sepsis involves activation of the vascular endothelium and leukocytes, resulting in the release of various mediators, e.g. cytokines, nitric oxide (NO), endothelin (ET-1) and complement factors. We evaluated the blood levels of complement activation, ET-1 and neuropeptide Y (NPY) in parallel with the haemodynamic and oxygen transport response during human experimental endotoxemia. METHODS: Eleven healthy men had venous, arterial and pulmonary arterial catheters placed for continuous haemodynamic measuring. After 30 min rest endotoxin (E. Coli 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 oxygen consumption and the tissue oxygen transport increased. Activation of the complement system was indicated by an increase in SC5b-9. Endothelin-1-like immunoreactivity (ET-1-LI) increased over time in arterial blood. NPY-like immunoreactivity (NPY-LI) 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-LI, illustrating that the model is a useful tool for inducing moderate systemic inflammation where several mediator systems are activated.

Subject headings and genre

Adult
Body Temperature
drug effects
Complement Activation
physiology
Endothelin-1
blood
Endotoxemia
physiopathology
Endotoxins
Hemodynamics
physiology
Humans
Inflammation
chemically induced
physiopathology
Male
Neuropeptide Y
blood
Oxygen Consumption
drug effects
Pulmonary Alveoli
metabolism
physiology
Pulmonary Gas Exchange
drug effects

Added entries (persons, corporate bodies, meetings, titles ...)

Albert, JKarolinska Institutet (author)
Weitzberg, EKarolinska Institutet (author)
Bengtsson, Anders,1954Gothenburg University,Göteborgs universitet,Institutionen för de kirurgiska disciplinerna, Avdelningen för anestesiologi och intensivvård,Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care(Swepub:gu)xbeand (author)
Lundberg, J O NKarolinska Institutet (author)
Sollevi, AKarolinska Institutet (author)
Karolinska InstitutetInstitutionen för de kirurgiska disciplinerna, Avdelningen för anestesiologi och intensivvård (creator_code:org_t)

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In:Acta anaesthesiologica Scandinavica: Wiley48:1, s. 74-810001-5172

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