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Prevention and/or treatment of ischemic stroke with nitric oxide synthase substrates
Author(s) -
Chiou George C.Y.,
Hong ShowJen
Publication year - 1997
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/(sici)1098-2299(199701)40:1<88::aid-ddr9>3.0.co;2-p
Subject(s) - nitric oxide synthase , ischemia , medicine , nitric oxide , stroke (engine) , cerebral blood flow , anesthesia , pharmacology , arginine , chemistry , biochemistry , mechanical engineering , amino acid , engineering
Previous studies have shown that nitric oxide (NO) synthase substrates such as L‐arginine and N α ‐benzoyl‐L‐arginine ethyl ester (BAEE) are capable of lowering intraocular pressure and improving ocular blood flow. Therefore, it is hoped that these agents could improve the cerebral blood flow after ischemic stroke and to prevent or reduce cerebral neuronal damages. Rat ischemic stroke was induced by an occlusion of middle cerebral artery and common carotid artery for 60 min. The occlusion was then released and the extent of neural damage was measured by the measurement of necrosis areas. L‐Arginine and BAEE were able to prevent neural damages by 99% and 94% respectively, at 1 h; 96% and 86%, respectively, at 6 h; and 90% and 77%, respectively, at 24 h after ischemia. A marked concentration‐response increase of c‐AMP was observed by both L‐arginine and BAEE in the cultured aortic A7r5 cells. These results indicate that NO synthase substrates are able to prevent/reduce ischemic stroke possibly through improvement of cerebral blood flow and via conservation of high energy phosphate compounds such as c‐AMP. Drug Dev. Res. 40:88–93, 1997. © 1997 Wiley‐Liss, Inc.