title: Electroacupuncture acutely improves cerebral blood flow and attenuates moderate ischemic injury via an endothelial mechanism in mice.
abstract: Electroacupuncture (EA) is a novel therapy based on traditional acupuncture combined with modern eletrotherapy that is currently being investigated as a treatment for acute ischemic stroke. Here, we studied whether acute EA stimulation improves tissue and functional outcome following experimentally induced cerebral ischemia in mice. We hypothesized that endothelial nitric oxide synthase (eNOS)-mediated perfusion augmentation was related to the beneficial effects of EA by interventions in acute ischemic injury. EA stimulation at Baihui (GV20) and Dazhui (GV14) increased cerebral perfusion in the cerebral cortex, which was suppressed in eNOS KO, but there was no mean arterial blood pressure (MABP) response. The increased perfusion elicited by EA were completely abolished by a muscarinic acetylcholine receptor (mAChR) blocker (atropine), but not a β-adrenergic receptor blocker (propranolol), an α-adrenergic receptor blocker (phentolamine), or a nicotinic acetylcholine receptor (nAChR) blocker (mecamylamine). In addition, EA increased acetylcholine (ACh) release and mAChR M3 expression in the cerebral cortex. Acute EA stimulation after occlusion significantly reduced infarct volume by 34.5% when compared to a control group of mice at 24 h after 60 min-middle cerebral artery occlusion (MCAO) (moderate ischemic injury), but not 90-min MCAO (severe ischemic injury). Furthermore, the impact of EA on moderate ischemic injury was totally abolished in eNOS KO. Consistent with a smaller infarct size, acute EA stimulation led to prominent improvement of neurological function and vestibule-motor function. Our results suggest that acute EA stimulation after moderate focal cerebral ischemia, but not severe ischemia improves tissue and functional recovery and ACh/eNOS-mediated perfusion augmentation might be related to these beneficial effects of EA by interventions in acute ischemic injury.
authors: Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam, Republic of Korea.
authors: Ji Hyun
authors: JH
authors: Kim
authors: Kyung Ha
authors: KH
authors: Choi
authors: Young Jung
authors: YJ
authors: Jang
authors: Sun Sik
authors: SS
authors: Bae
authors: Byung-Cheul
authors: BC
authors: Shin
authors: Byung Tae
authors: BT
authors: Choi
authors: Hwa Kyoung
authors: HK
authors: Shin
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D015669:Acupuncture Points; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000502:physiology; D002540:Cerebral Cortex / Q000098:blood supply / Q000187:drug effects / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D015671:Electroacupuncture / Q000379:methods*; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018727:Muscarinic Antagonists / Q000494:pharmacology; D052250:Nitric Oxide Synthase Type III / Q000235:genetics / Q000378:metabolism*; D043587:Receptor, Muscarinic M3 / Q000378:metabolism; D020127:Recovery of Function / Q000502:physiology; D015427:Reperfusion Injury / Q000503:physiopathology / Q000628:therapy*
chemical_list: D018727:Muscarinic Antagonists; D043587:Receptor, Muscarinic M3; D001285:Atropine; D052250:Nitric Oxide Synthase Type III; C496315:Nos3 protein, mouse; D000109:Acetylcholine