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Derangements of post-ischemic cerebral blood flow by protein kinase C delta

H W Lin1, R A Defazio, D Della-Morte

  • 1Cerebral Vascular Disease Research Center, Department of Neurology, University of Miami, Miller School of Medicine, Miami, FL 33136, USA.

Neuroscience
|September 4, 2010
PubMed

Insights

Protein kinase C delta (δPKC) inhibition reduces cerebral blood flow abnormalities after ischemia. This finding suggests δPKC may be a therapeutic target for stroke and related conditions.

Area of Science:

  • Neuroscience
  • Cerebrovascular Physiology
  • Ischemic Stroke Research

Background:

  • Cerebral ischemia causes abnormal blood flow, including hyperemia and hypoperfusion.
  • Protein kinase C delta (δPKC) is implicated in neuronal death post-ischemia.
  • The role of δPKC in regulating cerebral blood flow (CBF) after ischemia is unclear.

Purpose of the Study:

  • To investigate the role of δPKC in CBF derangements following cerebral ischemia.
  • To test the hypothesis that δPKC exacerbates hyperemia and subsequent hypoperfusion.

Main Methods:

  • Using Sprague-Dawley rats, researchers administered a specific δPKC inhibitor (δV1-1).
  • Cerebral blood flow changes were measured using 2-photon microscopy in a 2-vessel occlusion plus hypotension model.
  • Neuronal survival was assessed in an asphyxial cardiac arrest (ACA) model.

Main Results:

  • δPKC inhibition attenuated hyperemia and latent hypoperfusion, showing altered microvessel dynamics.
  • Treatment with δV1-1 improved cerebral perfusion 24 hours post-ACA.
  • Reduced hippocampal CA1 neuronal death was observed 7 days after ACA in treated rats.

Conclusions:

  • δPKC plays a significant role in modulating cerebral blood flow derangements after ischemic events.
  • Inhibiting δPKC demonstrates potential therapeutic benefits in reducing ischemic brain damage.
  • Targeting δPKC could be a novel strategy for managing cerebral ischemia.

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