Regional measurements of NO formedin vivoduring brain ischemia

Abstract

Nitric oxide formed in vivo in the rat brain regions of hippocampus, striatum, neocortex and cerebellum was spin trapped and measured ex vivo by cryogenic electron paramagnetic resonance spectroscopy. In non-ischemic control animals the rate of nitric oxide (NO) formation in the individual brain regions ranged from 15 to 42 pmol.g-1.min-1. During exposure to global ischemia for 7 min the generation of NO increased in all parts of the brain. In the hippocampus the rate of NO formation during ischemia increased by 6-fold from a control rate of 19 pmol.g-1.min-1. This increase was attenuated 47% by pretreatment with the NO synthase antagonist 7-nitroindazole, whereas pretreatment with the non-NMDA receptor anatogonist NBQX and the Ca2+ channel blocker NS638 did not influence the NO formation. The data show that short-duration ischemia elicits a significant, NO-synthase-dependent formation of NO in all brain regions.

Potential involvement of calcium and nitric oxide in protective effects of puerarin on oxygen–glucose deprivation in cultured hippocampal neurons

“…It was reported that nNOS and eNOS are extremely active at the very early stages, and iNOS is at the late stages of cerebral ischemia (>6 h) (Jiang et al, 2002). Olesen et al (1997) reported that 7 min after ligaturing the carotids an increase in NO was observed in hippocampus. Zhang et al reported an increase of NO at 2-6 min after middle cerebral artery occlusion and in the first 10 min of OGD in cultured hippocampus (Zhang et al, 1995(Zhang et al, , 2003.…”

Nitric Oxide Synthase in Acute Alteration of Nitric Oxide Levels after Subarachnoid Hemorrhage

“…We have previously shown that cerebral NO levels decrease immediately after SAH and subsequently increase (39). The transient decrease in NO makes SAH unique among all other forms of cerebral ischemia, in which an increase in NO is observed (8,21,25,26,30,31,48). The unique decrease in NO that occurs in SAH may contribute to several pathophysiological events, including unopposed vasoconstriction, decreased CBF, cerebral ischemia, and increased glutamate release (3,4,35,38), which together may augment brain injury after SAH.…”

Group I and Group III metabotropic glutamate receptor subtypes provide enhanced neuroprotection

“…One particular mechanism that contributes to PCD involves the free radical nitric oxide (NO). Generation of NO can lead to ischemia (Olesen et al, 1997), trauma (Yoon et al, 1996), and Alzheimer disease (Smith et al, 1998) through the induction of PCD. As a result, investigations of potential therapeutic targets have focused on the ability to modulate NO-induced PCD.…”