Increase in nitric oxide in the hypoxic–ischemic neonatal rat brain and suppression by 7-nitroindazole and aminoguanidine

• Published in: European journal of pharmacology Vol. 342; no. 1; pp. 47 - 49
• Main Authors: Higuchi, Yoshihisa, Hattori, Haruo, Kume, Toshiaki, Tsuji, Masahiro, Akaike, Akinori, Furusho, Kenshi
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 19.01.1998; Elsevier
• Subjects: 7-Nitroindazole; Aminoguanidine; Animals; Animals, Newborn; Biological and medical sciences; Brain Chemistry - drug effects; Brain Chemistry - physiology; Brain Ischemia - enzymology; Brain Ischemia - metabolism; Enzyme Induction - drug effects; Enzyme Inhibitors - pharmacology; Guanidines - pharmacology; Hypoxia, Brain - enzymology; Hypoxia, Brain - metabolism; Hypoxic–ischemic encephalopathy; Indazoles - pharmacology; Medical sciences; Neurology; Nitric oxide (NO); Nitric Oxide - metabolism; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase - biosynthesis; Nitric Oxide Synthase Type I; Nitric Oxide Synthase Type II; Rat, neonatal; Rats; Rats, Wistar; Time Factors; Vascular diseases and vascular malformations of the nervous system; 7-Nitroindazole; Aminoguanidine; Hypoxic–ischemic encephalopathy; Nitric oxide (NO); Rat, neonatal; Human; Nervous system diseases; Oxygen; Pathophysiology; Rat; Enzyme; Metabolite; Rodentia; Cardiovascular disease; Nitric-oxide synthase; Cerebral disorder; Vascular disease; Vertebrata; Mammalia; Newborn; Ischemia; Animal; Nitric oxide; Encephalopathy; Central nervous system disease; Hypoxia; Oxidoreductases; Cerebrovascular disease; Brain (vertebrata)
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/S0014-2999(97)01524-0

We measured the changes in nitric oxide (NO) metabolites in the brains of neonatal rats with hypoxic–ischemic damage. There were two peaks of NO metabolites in the lesioned side of the cortex without treatment: one during hypoxia and the other during the re-oxygenation period. Prehypoxic treatment with 7-nitroindazole, a selective neuronal NO synthase inhibitor, suppressed both peaks of NO metabolites, whereas prehypoxic treatment with aminoguanidine, a selective inducible NO synthase inhibitor, partially suppressed only the peak in the re-oxygenation period. These data suggest different roles of neuronal and inducible NO synthases in the pathogenesis of hypoxic–ischemic encephalopathy.