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Aminoguanidine does not influence tissue extravasation of albumin in endotoxaemic rats
Linköping University, Department of Medical and Health Sciences, Anesthesiology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Medical and Health Sciences, Anesthesiology. Linköping University, Faculty of Health Sciences.
2001 (English)In: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 45, no 1, 112-118 p.Article in journal (Refereed) Published
Abstract [en]

Background: It is generally maintained that protein and fluid are lost from the circulation under septic conditions. The role played by an increased production of nitric oxide, by the inducible nitric oxide synthase (iNOS), in this process is unclear.

Methods: Chloralose anaesthetised male Wistar rats received E. coli lipopolysaccharide (LPS), 3 mg kg−1 i.v., and were studied for 5 h. Mean arterial pressure (MAP) and heart rate (HR) were monitored and haematocrit (Hct) was determined intermittently. Tissue plasma volume and tissue clearances of radiolabelled albumin over the last 2 h of the experiment were determined by a double-isotope method. In 8 rats, 2 h after LPS, aminoguanidine, an iNOS selective blocker, was given i.v. at a dose of 5 mg kg−1. This was followed by a continuous infusion for the duration of the experiment; altogether 20 mg kg−1 was administered. In the control group (n=8), a corresponding volume of saline was infused.

Results: Aminoguanidine did not significantly influence Hct, MAP and HR, as evidenced by inter-group comparisons (Mann-Whitney test). Tissue plasma clearances of albumin and tissue plasma volume were similar in both groups.

Conclusion: Aminoguanidine at 20 mg kg−1 did not reverse the haemodynamic changes induced by LPS. Neither did the drug affect the tissue plasma clearance of albumin or the tissue plasma volume.

Place, publisher, year, edition, pages
2001. Vol. 45, no 1, 112-118 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-26995DOI: 10.1034/j.1399-6576.2001.450117.xLocal ID: 11631OAI: oai:DiVA.org:liu-26995DiVA: diva2:247546
Available from: 2009-10-08 Created: 2009-10-08 Last updated: 2017-12-13Bibliographically approved
In thesis
1. Nitric oxide and extravasation in endotoxaemia: an experimental study
Open this publication in new window or tab >>Nitric oxide and extravasation in endotoxaemia: an experimental study
2002 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Background: Despite advances in intensive care the mortality of patients in septic shock is still high. In early stages the condition is characterised by circulatory failure that is a consequence of myocardial depression, vasodilatation with decreased sensitivity to catecholamine stimulation and increased loss of protein and fluid from the circulation. For each of these components nitric oxide (NO) has been proposed as a mediator. In the thesis focus is on extravasation and the influence of NO on this.

Methods: As a model of sepsis chloralose anaesthetised rats were subjected to endotoxaernia induced by E. coli lipopolysaccharide (LPS) 3 mg kg-1 i.v. Mean arterial pressure (MAP), heart rate (HR) and haematocrit (Hct) were followed. NO synthesis was evaluated by the detection of methaemoglobin (metHb), nitrite and nitrate in blood. Extravasation was investigated by a double isotope method of labelled albumin (albumin clearance) and by the determination of extravascular water. The effects of endotoxaemia were studied for 3 or, in the majority of cases, 5 h. To evaluate, the involvement of inducible nitric oxide synthase (iNOS) aminoguanidine (AG), an inhibitor of iNOS was employed. Finally, the presence of iNOS in several tissues was investigated by immunohistochemistry.

Main Results: LPS increased formation of NO metabolites. Initially after LPS MAP was decreased and HR elevated. Het was decreased over the 5 h observation period. After LPS the leakage of albumin, as evidenced by albumin clearance, was decreased in several vascular beds, mostly in the gastrointestinal tract. Extravascular water was not increased in any tissue. AG had no influence on circulatory changes to LPS or on albumin clearance despite the inhibition of NO synthesis as indicated by metHb and nitrate. iNOS was present in several tissues of LPS treated as well as control rats but not in the heart or in any vessels; only in the lung was there a significant increase of iNOS positive inflammatory cells after LPS as compared to controls.

Conclusion: In this rat model of endotoxaemia LPS increased the formation of NO and induced circulatory changes commonly seen in rat endotoxaernia. Yet there were no signs of increased extravasation, on the contrary results are compatible with decreased or unchanged losses of fluid and albumin. It is proposed that this result is depending on changed microvascular haemodynamics. It also shows that increased NO formation does not necessarily lead to increased extravasation and indicates that NO could  protect against extravasation in endotoxaemia or at least be neutral for the process. It also points to the importance of carefully evaluating the experimental models used in the study of endotoxaemia.

Place, publisher, year, edition, pages
Linköping: Linköpings universitet, 2002. 85 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 728
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-27523 (URN)12179 (Local ID)91-7373-170-6 (ISBN)12179 (Archive number)12179 (OAI)
Public defence
2002-05-03, Berzeliussalen, Universitetssjukhuset, Linköping, 09:00 (Swedish)
Opponent
Available from: 2009-10-08 Created: 2009-10-08 Last updated: 2012-09-13Bibliographically approved

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