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The complement membrane attack complex and the bystander effect in cerebral vasospasm

C C Park1, M L Shin, J M Simard

  • 1Department of Neurosurgery, University of Maryland School of Medicine, Baltimore 21201, USA.

Journal of Neurosurgery
|August 1, 1997
PubMed
Summary
This summary is machine-generated.

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Complement activation by aged red blood cells forms membrane attack complexes (MACs). These MACs can damage nearby cells, potentially contributing to cerebral vasospasm after subarachnoid hemorrhage.

Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • Complement activation generates membrane attack complexes (MACs) capable of damaging cells.
  • The 'bystander effect' involves MACs damaging nearby cells, not directly involved in the initial activation.
  • Cerebral vasospasm after subarachnoid hemorrhage is a critical clinical concern.

Purpose of the Study:

  • To investigate the role of complement-mediated bystander effects in cerebral vasospasm.
  • To determine if aged erythrocytes can trigger complement activation leading to smooth muscle cell damage.

Main Methods:

  • Utilized a sensitive patch clamp technique to measure membrane conductance.
  • Compared the effects of aged versus fresh autologous erythrocytes on rat cerebral artery smooth muscle cells in the presence of autologous serum.

Related Experiment Videos

  • Manipulated complement pathways using heat inactivation, EGTA, and component-depleted sera.

    • Main Results:

    • Aged erythrocytes, but not fresh ones, significantly increased membrane conductance of smooth muscle cells.
    • This effect was complement-dependent, mediated via the classic pathway, and involved MACs.
    • MACs inserted into smooth muscle cell membranes, causing conductance changes consistent with the bystander effect.

    Conclusions:

    • Complement activation by aged erythrocytes can lead to MAC insertion into innocent bystander smooth muscle cells.
    • This novel mechanism may contribute to the pathophysiology of cerebral vasospasm following subarachnoid hemorrhage.