scholarly journals Inhibition of Vascular Nitric Oxide after Rat Chronic Brain Hypoperfusion: Spatial Memory and Immunocytochemical Changes

2005 ◽  
Vol 25 (6) ◽  
pp. 663-672 ◽  
Author(s):  
Jack C. de la Torre ◽  
Gjumrakch Aliev
Keyword(s):  
Nitric Oxide ◽  
Spatial Memory ◽  
Memory Function ◽  
Critical Role ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Significant Loss ◽  
Electron Microscopic ◽  
Vessel Occlusion ◽  
Common Carotid Artery Occlusion

An aging rat model of chronic brain hypoperfusion (CBH) that mimics human mild cognitive impairment (MCI) was used to examine the role of nitric oxide synthase (NOS) isoforms on spatial memory function. Rats with CBH underwent bilateral common carotid artery occlusion (2-vessel occlusion (2-VO)) for either 26 or 8 weeks and were compared with nonoccluded sham controls (S-VO). The neuronal and endothelial (nNOS/eNOS) constitutive inhibitor nitro-L-arginine methyl ester (L-NAME) 20 mg/kg was administered after 26 weeks for 3 days to 2-VO and S-VO groups and spatial memory was assessed with a modified Morris watermaze test. Only 2-VO rats worsened their spatial memory ability after L-NAME. Electron microscopic immunocytochemical examination using an antibody against eNOS showed 2-VO rats had significant loss or absence of eNOS-containing positive gold particles in hippocampal endothelium and these changes were associated with endothelial cell compression, mitochondrial damage and heavy amyloid deposition in hippocampal capillaries and perivascular region. In the 8-week study, three groups of 2-VO rats were administered an acute dose of 7-NI, aminoguanidine or L-NIO, the relatively selective inhibitors of nNOS, inducible NOS and eNOS. Only rats administered the eNOS inhibitor L-NIO worsened markedly their watermaze performance ( P=0.009) when compared with S-VO nonoccluded controls. We conclude from these findings that vascular nitric oxide derived from eNOS may play a critical role in spatial memory function during CBH possibly by keeping cerebral perfusion optimal through its regulation of microvessel tone and cerebral blood flow and that disruption of this mechanism can result in spatial memory impairment. These findings may identify therapeutic targets for preventing MCI and treating Alzheimer's disease.

scholarly journals Increased Sestrin3 Contributes to Post-ischemic Seizures in the Diabetic Condition

2021 ◽  
Vol 14 ◽  
Author(s):  
Zhongshan Shi ◽  
Zhigang Lei ◽  
Fan Wu ◽  
Luoxing Xia ◽  
Yiwen Ruan ◽  
...  
Keyword(s):  
Granule Cells ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Diabetic Rats ◽  
Electrophysiological Recording ◽  
Diabetic Mice ◽  
Membrane Excitability ◽  
Vessel Occlusion ◽  
Bilateral Common Carotid Artery ◽  
Common Carotid Artery Occlusion

Seizures are among the most common neurological sequelae of stroke, and diabetes notably increases the incidence of post-ischemic seizures. Recent studies have indicated that Sestrin3 (SESN3) is a regulator of a proconvulsant gene network in human epileptic hippocampus. But the association of SESN3 and post-ischemic seizures in diabetes remains unclear. The present study aimed to reveal the involvement of SESN3 in seizures following transient cerebral ischemia in diabetes. Diabetes was induced in adult male mice and rats via intraperitoneal injection of streptozotocin (STZ). Forebrain ischemia (15 min) was induced by bilateral common carotid artery occlusion, the 2-vessel occlusion (2VO) in mice and 4-vessel occlusion (4VO) in rats. Our results showed that 59% of the diabetic wild-type mice developed seizures after ischemia while no seizures were observed in non-diabetic mice. Although no apparent cell death was detected in the hippocampus of seizure mice within 24 h after the ischemic insult, the expression of SESN3 was significantly increased in seizure diabetic mice after ischemia. The post-ischemic seizure incidence significantly decreased in SESN3 knockout mice. Furthermore, all diabetic rats suffered from post-ischemic seizures and non-diabetic rats have no seizures. Electrophysiological recording showed an increased excitatory synaptic transmission and intrinsic membrane excitability in dentate granule cells of the rat hippocampus, together with decreased IA currents and Kv4.2 expression levels. The above results suggest that SESN3 up-regulation may contribute to neuronal hyperexcitability and seizure generation in diabetic animals after ischemia. Further studies are needed to explore the molecular mechanism of SESN3 in seizure generation after ischemia in diabetic conditions.

Recanalization of Acute Common Carotid Artery Occlusion: 2-Dimensional Operative Video

2018 ◽  
Vol 16 (5) ◽  
pp. 633-633 ◽  
Author(s):  
Thomas J Sorenson ◽  
Harry Cloft ◽  
Alejandro Rabinstein ◽  
Giuseppe Lanzino
Keyword(s):  
Carotid Artery ◽  
Common Carotid Artery ◽  
Internal Carotid ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Vessel Occlusion ◽  
Major Vessel ◽  
Common Carotid Artery Occlusion ◽  
Treatment Risks ◽  
Major Stroke

Abstract While revascularization of the acutely or chronically occluded internal carotid artery has become commonplace with modern endovascular techniques, revascularization of an acutely occluded common carotid artery (CCA) is a controversial procedure with unique challenges. These challenges can be related to the lack of observable markers for identifying vessels during navigation or for identifying the exact location and extent of occlusion within the CCA, in addition to wide-ranging treatment risks. In this video, we illustrate the controversial revascularization of a 68-yr-old woman with an acute CCA occlusion who presented with fluctuating neurological symptoms. We believed treatment to be indicated by the lack of adequate collaterals on the intracranial CTA, and fluctuating symptoms in the absence of an intracranial major vessel occlusion, suggesting that the CCA occlusion was exerting important hemodynamic effects and at risk of causing a major stroke without revascularization, despite a low initial NIH stroke score. Though acute recanalization of patients with low NIH stroke score with stent-angioplasty is a controversial procedure, we believed it to be necessary in the case of our patient and believe it will likely be the focus of the next wave of large clinical trials dedicated to acute stroke.

scholarly journals iNOS-Derived NO and Nox2-Derived Superoxide Confer Tolerance to Excitotoxic Brain Injury through Peroxynitrite

2007 ◽  
Vol 27 (8) ◽  
pp. 1453-1462 ◽  
Author(s):  
Takayuki Kawano ◽  
Alexander Kunz ◽  
Takato Abe ◽  
Hélène Girouard ◽  
Josef Anrather ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Brain Injury ◽  
Nadph Oxidase ◽  
Cortical Neurons ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
No Donor ◽  
Inos Inhibitor ◽  
Common Carotid Artery Occlusion

Sublethal injurious stimuli induce tolerance to subsequent lethal insults, a phenomenon termed preconditioning. Inducible nitric oxide synthase (iNOS) is essential for the preconditioning induced by transient bilateral common carotid artery occlusion (BCCAO) or by systemic administration of the endotoxin lipopolysaccharide (LPS). We used a model of brain injury produced by neocortical injection of N-methyl-d-aspartate (NMDA) to investigate the mechanisms by which iNOS-derived nitric oxide (NO) contributes to tolerance induced by LPS or BCCAO. We found that the tolerance is blocked by the iNOS inhibitor aminoguanidine, is not observed in iNOS-null mice, and is rescued by the NO donor DTPA NONOate. Lipopolysaccharide failed to induce preconditioning in mice lacking the nox2 subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, suggesting that superoxide derived from NADPH oxidase is needed for the induction of the tolerance. Because superoxide reacts with NO to form peroxynitrite, we investigated the role of peroxynitrite. We found that LPS induces the peroxynitrite marker 3-nitrotyrosine in cortical neurons and that the peroxynitrite decomposition catalyst FeTPPS abolishes LPS-induced preconditioning. These results suggest that the protective effect of iNOS-derived NO is mediated by peroxynitrite formed by the reaction of NO with NADPH oxidase-derived superoxide. Thus, peroxynitrite, in addition to its well-established deleterious role in ischemic brain injury and neurodegeneration, can also be beneficial by inducing tolerance to excitotoxicity.

Spontaneous temperature changes in the 2-vessel occlusion model of cerebral ischemia in rats

2007 ◽  
Vol 85 (12) ◽  
pp. 1263-1268 ◽  
Author(s):  
Darren L. Clark ◽  
Maxine DeButte-Smith ◽  
Frederick Colbourne
Keyword(s):  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Vessel Occlusion ◽  
Temperature Changes ◽  
Physiological Variables ◽  
Bilateral Common Carotid Artery ◽  
Hippocampal Ca1 ◽  
Before And After ◽  
Highly Correlated ◽  
Common Carotid Artery Occlusion

Transient global ischemia (ISC) in rats and humans causes selective and delayed neuronal death in the hippocampal CA1 sector. It is clear from rodent studies that hyperthermia aggravates, whereas hypothermia lessens, this injury. In this study we sought to relate core (Tc) and brain (Tb) temperature, measured via telemetry probes, after ISC produced in rats by bilateral common carotid artery occlusion combined with systemic hypotension (2-VO model). We also tested whether spontaneous postischemic temperature fluctuations occurred and whether they were related to cell death as previous studies indicate. We report that Tc and Tb readings are similar and are highly correlated before and after 10 min of 2-VO ISC. In the second experiment, rats were subjected to 8, 9, or 10 min of 2-VO ISC. Despite a range in CA1 injury among these animals, there was no evidence of post-ISC hyperthermia, contrary to earlier work, and neither temperature nor the physiological variables measured during ISC (e.g., glucose) predicted injury. Our findings suggest that, under the present conditions, 2-VO rats do not experience postoperative hyperthermia, which can be adequately measured with Tc telemetry probes.

scholarly journals Common Carotid Artery Occlusion Treatment: Revealing a Gap in the Current Guidelines

2013 ◽  
Vol 58 (3) ◽  
pp. 846 ◽  
Author(s):  
C. Klonaris ◽  
G.N. Kouvelos ◽  
M. Kafeza ◽  
A. Koutsoumpelis ◽  
A. Katsargyris ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Common Carotid Artery ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Common Carotid Artery Occlusion ◽  
Current Guidelines
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