Effects of Nitric Oxide Synthase Inhibition on Cerebral Blood Flow following Bilateral Carotid Artery Occlusion and Recirculation in the Rat

Prado, Ricardo; Watson, Brant D.; Wester, Per

doi:10.1038/jcbfm.1993.91

Cited by 54 publications

(15 citation statements)

References 13 publications

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“…By contrast, a large body of evidence has suggested that the gaseous mediator nitric oxide (NO), crucially involved in the pathophysiological mechanism of brain damage under ischemic conditions, can act either as a neuroprotective agent (Morikawa et al . 1992; Prado et al . 1993) or as a neurodetrimental second messenger (Iadecola et al .…”

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confidence: 99%

HIF‐1α reveals a binding activity to the promoter of iNOS gene after permanent middle cerebral artery occlusion

Matrone

Pignataro

Molinaro

et al. 2004

Journal of Neurochemistry

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Hypoxia inducible factor (HIF-1)-1a is a specific, oxygensensitive protein that regulates the activity of HIF-1, a transcriptional factor that increases after cerebral ischemia and may either promote or prevent neuronal survival. In this study to determine whether the inducible nitric oxide synthase (iNOS) gene containing the sequence of the hypoxiaresponsive enhancer (HRE) was an HIF-1 target after cerebral ischemia induced by permanent middle cerebral artery occlusion (pMCAO), electrophoretic mobility shift assay (EMSA) and iNOS western blot analysis were performed in the ischemic core, in the area surrounding the infarct and in the hippocampus ipsilateral and contralateral to the lesion. In addition, both HIF-1a mRNA and protein expression were examined in the ischemic core, in the area surrounding the ischemic core and in the hippocampus ipsilateral to the insult. Our results revealed that pMCAO up-regulates iNOS protein in the ischemic core, in the area surrounding the ischemic core and in the hippocampus ipsilateral to the lesion, and that the activation of iNOS expression is mediated by HIF-1. Moreover, HIF-1a mRNA and protein levels increased in the ischemic core and in the hippocampus ipsilateral to the lesion compared with the levels obtained in the corresponding areas of sham-operated controls or in the contralateral hemisphere. Particularly in the area surrounding the ischemic core, HIF-1a protein accumulated during pMCAO although mRNA did not increase. Our study suggests that the activation of HIF-1 might be involved in the mechanisms whereby iNOS promotes cell survival and/or death after cerebral ischemia. Keywords: hippocampus, hypoxia inducible factor-1, inducible nitric oxide synthase, inducible nitric oxide synthase promoter, ischemia, pMCAO.

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confidence: 99%

HIF‐1α reveals a binding activity to the promoter of iNOS gene after permanent middle cerebral artery occlusion

Matrone

Pignataro

Molinaro

et al. 2004

Journal of Neurochemistry

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“…However, the postischemic reduction in CBF in the L-NAMEtreated groups compared with the saline-treated group was less severe than what has been reported in L-NAME-treated rats after bilateral carotid occlusion. 42 Taken together these studies indicate that the mechanism for decreased striatal injury after transient focal ischemia by L-NAME is not due to improved distribution of blood flow during MCA occlusion or reperfusion.…”

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confidence: 72%

Nitric oxide synthase inhibition reduces caudate injury following transient focal ischemia in cats.

Nishikawa

Kirsch

Koehler

et al. 1994

Stroke

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Background and PurposeWe tested the hypothesis that inhibiting nitric oxide production either before or during transient focal ischemia affects early postischemic brain injury.Methods Halothane-anesthetized cats underwent 1 hour of left middle cerebral artery occlusion plus 3 hours of reperfusion. Pretreatment groups received either intravenous N"-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg, n=10) or an equal volume of diluent (10 mL saline, n=10) over 30 minutes before ischemia. Posttreatment groups received intravenous L-NAME (10 mg/kg) over 30 minutes from 45 minutes of ischemia to 15 minutes of reperfusion (n=10) or intravenous L-NAME (10 mg/kg) plus L-arginine (200 mg/kg) over the same period followed by continuous L-arginine infusion (200 mg/kg per hour) for the remainder of reperfusion (n=10).Results Microsphere-determined blood flow to ipsilateral caudate nucleus and inferior temporal cortex decreased to the same extent during ischemia and recovered to the same extent during reperfusion in the four groups. Triphenyltetrazoliumdetermined injury volume of ipsilateral caudate nucleus in cats

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“…N G ‐Nitro‐ l ‐arginine methyl ester, a NOS inhibitor, protects the brain following BCCAO. Increased cerebrovascular resistance and reduced cerebral blood flow occur during the ischaemic and reperfusion periods in l ‐NAME‐treated animals 3,27 . Our previous study 17 demonstrated that administration of l ‐NAME induced hypertension and suppressed NO release in the NTS.…”

Section: Discussionmentioning

confidence: 94%

“…Increased cerebrovascular resistance and reduced cerebral blood flow occur during the ischaemic and reperfusion periods in L-NAME-treated animals. 3,27 Our previous study 17 demonstrated that administration of L-NAME induced hypertension and suppressed NO release in the NTS. The effects of L-arginine on cardiovascular responses and NO release were attenuated by L-NAME pretreatment.…”

Section: Discussionmentioning

confidence: 98%

Nitric Oxide Release in the Nucleus Tractus Solitarius During and After Bilateral Common Carotid Artery Occlusion

Chai

2004

Clin Exp Pharma Physio

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1. The purpose of the present study was to investigate the effect of bilateral common carotid artery occlusion (BCCAO) on cardiovascular responses and nitric oxide (NO) formation in the nucleus tractus solitarius (NTS). 2. Twenty-three adult cats were anaesthetized intraperitoneally with urethane (400 mg/kg) and alpha-chloralose (40 mg/kg). The femoral artery was cannulated to allow monitoring of systemic arterial pressure (SAP) and heart rate (HR). The femoral vein was cannulated for intravenous drug administration. 3. Extracellular NO levels in the NTS were measured by in vivo voltammetry using an NO microsensor combined with a microcomputer-controlled apparatus. 4. Microinjection of l-arginine (30 nmol) into the NTS produced hypotension and NO release. This effect of l-arginine was not changed by 2 min of BCCAO. 5. Bilateral common carotid artery occlusion produced increases in SAP and NO levels. These effects were more apparent in vagotomized than in intact animals. 6. The onset latency of BCCAO-induced changes in SAP levels (8.4 +/- 2.5 s) was longer than that for changes in NO (4.7 +/- 1.7 s). 7. Bilateral common carotid artery occlusion induced hypertension and NO release in the NTS of intact and vagotomized animals. These cardiovascular and NO responses to BCCAO were significantly attenuated by NG-nitro-l-arginine methyl ester (10 mg/kg, i.v.) and MK-801 (2.5 mg/kg, i.v.). These data suggest that NO synthase and activation of N-methyl-d-aspartate receptors are involved in the cardiovascular and NO responses to BCCAO.

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Effects of Nitric Oxide Synthase Inhibition on Cerebral Blood Flow following Bilateral Carotid Artery Occlusion and Recirculation in the Rat

Cited by 54 publications

References 13 publications

HIF‐1α reveals a binding activity to the promoter of iNOS gene after permanent middle cerebral artery occlusion

HIF‐1α reveals a binding activity to the promoter of iNOS gene after permanent middle cerebral artery occlusion

Nitric oxide synthase inhibition reduces caudate injury following transient focal ischemia in cats.

Nitric Oxide Release in the Nucleus Tractus Solitarius During and After Bilateral Common Carotid Artery Occlusion

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