Interruption of perivascular sympathetic nerves of cerebral arteries offers neuroprotection against ischemia

Reggie H. Lee, Alexandre Couto e Silva, Francesca M. Lerner, Carl S. Wilkins, Stephen E. Valido, Daniel D. Klein, Celeste Y. Wu, Jake T. Neumann, David Della-Morte, Stephen H. Koslow, Alireza Minagar, Hung Wen Lin

Research output: Contribution to journalArticlepeer-review

Abstract

Sympathetic nervous system activity is increased after cardiopulmonary arrest, resulting in vasoconstrictor release from the perivascular sympathetic nerves of cerebral arteries. However, the pathophysiological function of the perivascular sympathetic nerves in the ischemic brain remains unclear. A rat model of global cerebral ischemia (asphyxial cardiac arrest, ACA) was used to investigate perivascular sympathetic nerves of cerebral arteries via bilateral decentralization (preganglionic lesion) of the superior cervical ganglion (SCG). Decentralization of the SCG 5 days before ACA alleviated hypoperfusion and afforded hippocampal neuroprotection and improved functional outcomes. These studies can provide further insights into the functional mechanism (s) of the sympathetic nervous system during ischemia. NEW & NOTEWORTHY Interruption of the perivascular sympathetic nerves can alleviate CA-induced hypoperfusion and neuronal cell death in the CA1 region of the hippocampus to enhance functional learning and memory.

Original languageEnglish (US)
Pages (from-to)H182-H188
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume312
Issue number1
DOIs
StatePublished - 2017
Externally publishedYes

Keywords

  • Behavior (rodent)
  • Brain ischemia
  • Cardiac arrest
  • Cerebral blood flow
  • Cerebral blood flow measurement
  • Cognitive impairment
  • Global ischemia
  • Neuroprotection
  • Pial vessels
  • Sympathetic nervous system
  • Two photon microscopy

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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