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Nitric oxide does not cause extravasation in endotoxemic rats
Kerstin Metcalf1, Anna Berg, Ann-Charlott Ericson
1Department of Medicine and Care, Division of Anaesthesiology and Clinical Research Center, University of Linköping, Linköping, Sweden. kerstin.metxalf@lio.se
The Journal of Trauma
|May 28, 2005
Summary
This study found that lipopolysaccharide (LPS) administration in rats did not increase vascular permeability or albumin leakage after 5 hours. These findings challenge the established role of nitric oxide (NO) in endotoxemia-induced vascular damage.
Area of Science:
- Physiology
- Pathophysiology
- Immunology
Background:
- Nitric oxide (NO) produced by inducible NO synthase (iNOS) is widely believed to increase vascular permeability during sepsis and endotoxemia.
- This study investigates the direct effects of endotoxin on vascular permeability and NO production.
Purpose of the Study:
- To evaluate the impact of lipopolysaccharide (LPS) on vascular permeability and albumin extravasation in a rat model of endotoxemia.
- To examine the role of inducible NO synthase (iNOS) in endotoxin-induced vascular changes.
Main Methods:
- Anesthetized rats were administered lipopolysaccharide (LPS) or saline (control) and observed for 5 hours.
- Measurements included mean arterial blood pressure, heart rate, hematocrit, transcapillary albumin exchange, tissue water content, and immunohistochemistry for nitric oxide synthase (NOS).
Main Results:
- LPS administration did not lead to increased albumin extravasation in the intestine or elevated tissue water content.
- Immunohistochemistry revealed similar endothelial and neuronal NOS staining in both LPS and control groups.
- A significant increase in iNOS-positive inflammatory cells was observed in the lungs of LPS-treated rats, but not in vascular structures or the heart.
Conclusions:
- At 5 hours post-LPS, there was no evidence of increased vascular leakage of water or albumin.
- These results question the prevailing hypothesis that NO is a primary mediator of vascular damage and extravasation in endotoxemia.