Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 312, Issue 1, Pages H182-H188Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00482.2016
Keywords
cardiac arrest; global ischemia; two photon microscopy; sympathetic nervous system; pial vessels; neuroprotection; cerebral blood flow; cerebral blood flow measurement; brain ischemia; behavior (rodent); cognitive impairment
Funding
- American Heart Association [AHA-13SDG1395001413]
- Louisiana State University grant-in-aid research council
- Evelyn F. McKnight Brain Institute
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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.
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