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Hindlimb ischemia-reperfusion increases complement deposition and glycolysis
1Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts, 02115, USA.
The Journal of Surgical Research
|June 29, 1999
Summary
Hindlimb ischemia-reperfusion (HIR) impairs muscle energy metabolism and causes injury. Complement deposition, not glutathione levels, correlated with muscle damage and bioenergetic changes after HIR.
Area of Science:
- Physiology
- Biochemistry
- Pathology
Background:
- Hindlimb ischemia-reperfusion (HIR) is known to disrupt cellular energy metabolism.
- Potential mechanisms include free radical or complement-mediated pathways contributing to muscle injury.
Purpose of the Study:
- To investigate the relationship between myocellular energetics, histopathological injury, and mediator activity in HIR.
- To assess the impact of varying degrees of HIR on muscle energy status and damage.
Main Methods:
- Male Wistar rats underwent 4 hours of ischemia followed by 4 hours of reperfusion (Sham, Unilateral, or Bilateral HIR).
- 31P magnetic resonance spectroscopy measured high-energy phosphate ratios (ATP/Pi, PCr/Pi).
- Muscle tissue analysis included histopathology, complement membrane attack complex (MAC) deposition, glutathione (GSH) levels, and enzyme activities.
Main Results:
- HIR significantly decreased ATP/Pi and PCr/Pi ratios, indicating impaired energy status and capacity.
- Increased severity of HIR correlated with greater MAC deposition and histological muscle damage.
- While GSH levels were unchanged, phosphofructokinase activity increased, suggesting glycolytic compensation. Myocellular bioenergetic alterations paralleled complement deposition more closely than GSH depletion.
Conclusions:
- Complement deposition is closely associated with skeletal muscle injury and compensatory metabolic changes following HIR.
- Therapeutic strategies targeting complement activity and bioenergetic assessment may improve the understanding and management of HIR injury.