Early nitric oxide increase in depolarized tissue of cat focal cerebral ischaemia.
Tissue nitric oxide (NO) concentration was investigated in relation to ion-homeostasis disturbance in the cat model of focal cerebral ischaemia. An NO electrode, a Ca2+ microelectrode and a laser Doppler probe were applied to the cerebral cortex in the core and periphery of the middle cerebral artery. NO concentration increased by 25.1 +/- 6.3 nM at 5 min in severely ischaemic regions exhibiting anoxic depolarization (n = 5, p < 0.0005). This occurred with no reduction in extracellular Ca2+ concentration and before a massive Ca2+ influx into cells started several minutes later. The NO increase was abolished by NG-nitro-L-arginine treatment (n = 6, p < 0.05) and was absent in regions with no depolarization (n = 5, p < 0.0005). We conclude that the early increase in NO associated with depolarization is achieved by activation of constitutive NO synthase, possibly triggered by intracellular Ca2+ release.
Ohta
K
K
Max-Planck-Institut für neurologische Forschung, Cologne, Germany.
Graf
R
R
Rosner
G
G
Kumura
E
E
Heiss
W D
WD
D000208:Acute Disease; D000818:Animals; D015374:Biosensing Techniques; D001794:Blood Pressure / Q000502:physiology; D001831:Body Temperature / Q000187:drug effects / Q000502:physiology; D002545:Brain Ischemia / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D002415:Cats; D002560:Cerebrovascular Circulation / Q000502:physiology; D004594:Electrophysiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D005260:Female; D002534:Hypoxia, Brain / Q000503:physiopathology*; D017078:Laser-Doppler Flowmetry; D008839:Microelectrodes; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000494:pharmacology
D004791:Enzyme Inhibitors; D019335:Nitroarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D002118:Calcium