| Literature DB >> 27864234 |
Reggie H Lee1,2,3, Alexandre Couto E Silva1,2,3, Francesca M Lerner1,2, Carl S Wilkins4, Stephen E Valido1,2, Daniel D Klein1,2, Celeste Y Wu2,3, Jake T Neumann5, David Della-Morte2,6,7, Stephen H Koslow8, Alireza Minagar3, Hung Wen Lin9,2,3.
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.Entities:
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
Mesh：
Year: 2016 PMID： 27864234 DOI： 10.1152/ajpheart.00482.2016
Source DB: PubMed Journal: Am J Physiol Heart Circ Physiol ISSN： 0363-6135 Impact factor: 4.733