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Systemic complement activation produces hemodynamic changes characteristic of sepsis.
W J Schirmer1, J M Schirmer, G B Naff
1Department of Surgery, Veterans Administration Medical Center, Cleveland, OH 44106.
Archives of Surgery (Chicago, Ill. : 1960)
|March 1, 1988
Summary
Systemic complement activation via zymosan in rats mimicked sepsis, causing initial hemodynamic changes and hepatic hypoperfusion. While systemic measures normalized, liver blood flow worsened over time, suggesting complement
Area of Science:
- Physiology
- Immunology
Background:
- Systemic complement activation can lead to sepsis-like hemodynamic changes.
- Understanding the role of complement in organ perfusion is crucial for treating sepsis and trauma.
Purpose of the Study:
- To investigate the hemodynamic effects of systemic complement activation induced by zymosan in rats.
- To examine the early and delayed effects of complement activation on systemic, hepatic, and renal blood flow.
Main Methods:
- Zymosan was administered intravenously to Sprague-Dawley rats in graded doses.
- Hemodynamic parameters, including cardiac output, mean arterial pressure, and blood flows, were measured at 2, 24, and 48 hours.
- Total hemolytic complement activity was assessed to confirm complement activation.
Main Results:
- Zymosan induced dose-dependent hemodynamic changes resembling hyperdynamic sepsis, including hepatic hypoperfusion.
- Systemic hemodynamic measures normalized by 24 and 48 hours post-administration.
- Liver blood flow remained depressed and worsened over time, while renal perfusion decreased at 48 hours.
Conclusions:
- Complement activation mediates systemic and visceral blood flow abnormalities.
- These abnormalities may precede and contribute to organ failure in sepsis and trauma.
- Complement's role in organ hypoperfusion highlights its potential as a therapeutic target.