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Complement activation during hemorrhagic shock and resuscitation in swine
Janos Szebeni1, Lajos Baranyi, Sandor Savay
1Department of Membrane Biochemistry, Walter Reed Army Institute of Research, Washington, DC 20307, USA. janos.szebeni@na.amedd.army.mil
Shock (Augusta, Ga.)
|September 23, 2003
Summary
Hemorrhagic shock, even without trauma, activates the complement system due to lactic acidosis and endotoxemia. This activation contributes to shock severity, with complex complement changes observed during resuscitation.
Area of Science:
- Immunology
- Physiology
- Trauma Research
Background:
- Complement (C) cascade activation is implicated in trauma-induced immune responses.
- The role of hypovolemia alone in C activation remains unclear.
Purpose of the Study:
- To investigate C activation in a porcine model of hemorrhagic shock without trauma.
- To determine the kinetics and causes of C activation during hypovolemia and resuscitation.
Main Methods:
- Hemorrhagic shock induced in pigs (35 mmHg for 90 min) followed by resuscitation.
- Measurement of complement factors (CH50/mL, C5a), thromboxane B2, and lipopolysaccharide (LPS).
- In vitro studies assessing C activation under lactic acidosis conditions.
Main Results:
- Significant C activation occurred during shock, preceding resuscitation.
- Lactic acidosis and increased LPS correlated with C activation.
- Resuscitation with plasma expanders increased C consumption, while whole blood improved CH50/mL.
Conclusions:
- Hypovolemia-induced lactic acidosis and endotoxemia trigger C activation, potentially worsening shock.
- The biphasic changes in complement levels suggest complex physiological responses to hemorrhage.
- Understanding C activation pathways is crucial for managing shock.