scholarly journals Downstream Microvascular Thrombosis in Cortical Venules Is an Early Response to Proximal Cerebral Arterial Occlusion

2018 ◽  
Vol 7 (5) ◽  
Author(s):  
Jean‐Philippe Desilles ◽  
Varouna Syvannarath ◽  
Lucas Di Meglio ◽  
Célina Ducroux ◽  
William Boisseau ◽  
...  
Keyword(s):  
Arterial Occlusion ◽  
Early Response ◽  
Microvascular Thrombosis ◽  
Cerebral Arterial Occlusion

Middle cerebral arterial occlusion in a child with osteopetrosis major

2001 ◽  
Vol 11 (1) ◽  
pp. 145-147 ◽  
Author(s):  
H. A. Tasdemir ◽  
A. Dagdemir ◽  
C. Celenk ◽  
D. Albayrak
Keyword(s):  
Arterial Occlusion ◽  
Cerebral Arterial Occlusion

L-arginine decreases infarct size caused by middle cerebral arterial occlusion in SHR

1992 ◽  
Vol 263 (5) ◽  
pp. H1632-H1635 ◽  
Author(s):  
E. Morikawa ◽  
Z. Huang ◽  
M. A. Moskowitz
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Focal Cerebral Ischemia ◽  
Arterial Occlusion ◽  
Cerebral Blood Vessels ◽  
Hypertensive Rats ◽  
Vessel Occlusion ◽  
Spontaneously Hypertensive ◽  
Cerebral Arterial Occlusion ◽  
Carotid Arterial

L-Arginine, but not D-arginine, serves as a precursor for the synthesis of nitric oxide (NO), a potent dilator of cerebral blood vessels. We examined the effects of administering L-arginine (300 mg/kg ip) on the volume of infarction in two models of focal cerebral ischemia in spontaneously hypertensive rats (SHR). L-Arginine was administered before (16 and 3 h) and after (5 min and 2 h) vessel occlusion, and animals were killed 24 h later. L-Arginine treatment decreased infarct size in rats subjected to distal middle cerebral arterial (MCA) plus ipsilateral common carotid arterial (CCA) occlusion by 31% [147 +/- 12 (saline) vs. 101 +/- 9 mm3 (L-arginine), P < 0.05]. D-Arginine, administered according to the same dosage and protocol, was without effect. In the group subjected to proximal MCA occlusion, L-arginine decreased infarction size in the striatum by 28% [47 +/- 5 (saline) vs. 34 +/- 3 mm3 (L-arginine), P < 0.05] and neocortex by 11% [193 +/- 7 (saline) vs. 171 +/- 8 mm3 (L-arginine), P < 0.05]. Changes in blood pressure or other measured physiological parameters did not account for the observed differences. The possible use of L-arginine for the treatment of focal cerebral ischemia merits further investigation.

Hypervolemic hemodilution in experimental focal cerebral ischemia

1983 ◽  
Vol 59 (3) ◽  
pp. 500-509 ◽  
Author(s):  
James H. Wood ◽  
Frederick A. Simeone ◽  
Eugene A. Fink ◽  
Michael A. Golden
Keyword(s):  
Molecular Weight ◽  
Focal Cerebral Ischemia ◽  
Arterial Occlusion ◽  
Total Blood ◽  
Content Type ◽  
Arterial Blood ◽  
Hypervolemic Hemodilution ◽  
The Mean ◽  
Cerebral Arterial Occlusion ◽  
Hemispheric Infarction

✓ Cerebrovascular and cardiac alterations evoked by intravascular volume expansion with low molecular weight dextran (LMD, molecular weight 40,000), an advocated adjunct in the clinical prevention or therapy of acute stroke and cerebral vasospasm, were studied in splenectomized dogs. Clipping of the right distal internal carotid artery and the proximal middle cerebral artery (MCA) in eight dogs decreased regional cortical blood flow (rCoBF) by 58% without changing cardiac output (CO), and caused 10% ± 5% (SE) hemispheric infarction. Ten other dogs underwent similar cerebral arterial occlusion and were infused twice with LMD within 2 hours; each infusion equaled 20% of the respective dog's total blood volume. Both CO and rCoBF in the territory of the occluded MCA increased significantly by 119% ± 13% and 42% ± 6%, respectively, following the two LMD infusions. Although the mean arterial blood pressure was unaltered, the hematocrit decreased significantly and the intracranial pressure (ICP) increased significantly. The mean hemispheric infarction in these 10 treated dogs was 4% ± 2%. Another nine dogs underwent arterial manipulation without clipping. Two hemodiluting LMD infusions, similar to those in the 10 dogs, significantly elevated CO and ICP but not rCoBF. These data suggest that hypervolemic hemodilution with LMD effectively elevates collateral perfusion to ischemic regions of brain distal to occluded MCA segments and concomitantly raises the CO and ICP.

scholarly journals "Low perfusion hyperemia" following middle cerebral arterial occlusion in cats of different age groups.

Stroke ◽  
1980 ◽  
Vol 11 (6) ◽  
pp. 629-636 ◽  
Author(s):  
M Tomita ◽  
F Gotoh ◽  
T Amano ◽  
N Tanahashi ◽  
K Tanaka
Keyword(s):  
Age Groups ◽  
Arterial Occlusion ◽  
Cerebral Arterial Occlusion

scholarly journals Measurement of cerebrovascular reserve by multimodal imaging for cerebral arterial occlusion or stenosis patients: protocol of a prospective, randomized, controlled clinical trial

2019 ◽  
Author(s):  
xiao zhipeng ◽  
ji ke ◽  
lin yong ◽  
wan jieqing ◽  
pan yaohua ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Ischemic Stroke ◽  
Arterial Occlusion ◽  
Transluminal Angioplasty ◽  
Cerebrovascular Reactivity ◽  
Stroke Recurrence ◽  
Controlled Clinical Trial ◽  
Cerebrovascular Reserve ◽  
Randomized Controlled ◽  
Cerebral Arterial Occlusion

Abstract Background Cerebrovascular reactivity (CVR), index of cerebral hemodynamics, might guide the treatment of ischemic stroke. However, the previous studies that the therapeutic strategy of stroke mainly depends on the degree of vascular stenosis with steady-state vascular parameters, such as cerebral blood flow, and CVR factors are not under consideration. Measurement of CVR by multimodal image might improve the prognosis for ischemic stroke. Methods/design The study is a prospective, randomized, paralleled controlled clinical trial to examine the multimodal image evaluation for CVR. A total of 66 eligible patients will be recruited from Renji hospital, Shanghai Jiaotong University School of Medicine. The patients will be categorized based on CVR into two subgroups as follows: CVR>10% group and CVR<10% group. And the patients will be randomly assigned to medical management, percutaneous transluminal angioplasty and stenting, and intracranial and extra-cranial bypass groups in a 1:1:1 ratio. The primary end point is all adverse events and ipsilateral stroke recurrence at 6, 12, 24 months after the management. The secondary outcomes include the CVR, the National Institute of Health stroke scale and the Modified Rankin Scale at 6, 12, 24 months. Discussion Measurement of cerebrovascular reserve by multimodal image is recommended by most recent studies to guide the treatment of ischemic stroke, and thus its efficacy and evaluation accuracy need to be established in randomized controlled settings. This prospective, randomized, paralleled controlled registry study, together with other ongoing studies, will present more evidence for optimal individualized accurate treatment of ischemic stroke.

scholarly journals Postconditioning with Isoflurane Reduced Ischemia-induced Brain Injury in Rats

2008 ◽  
Vol 108 (6) ◽  
pp. 1055-1062 ◽  
Author(s):  
Jeong Jin Lee ◽  
Liaoliao Li ◽  
Hae-Hyuk Jung ◽  
Zhiyi Zuo
Keyword(s):  
Potassium Channel ◽  
Brain Ischemia ◽  
Adult Male ◽  
Channel Blocker ◽  
Brain Slices ◽  
Arterial Occlusion ◽  
Sprague Dawley ◽  
Potassium Channel Blocker ◽  
Sprague Dawley Rats ◽  
Cerebral Arterial Occlusion

Background Preexposure of brain to isoflurane, a commonly used anesthetic, induces ischemic tolerance. This phenomenon is called isoflurane preconditioning. However, it is not known whether isoflurane application after ischemia provides neuroprotection. Methods Corticostriatal slices (400 microm) freshly prepared from adult male Sprague-Dawley rats were subjected to a 15-min oxygen-glucose deprivation (OGD; to simulate ischemia in vitro). Isoflurane was applied after OGD. Brain slices were harvested 2 h after OGD for measuring 2,3,5-triphenyltetrazolium chloride (TTC) conversion to quantify cell injury. Adult male Sprague-Dawley rats were also subjected to middle cerebral arterial occlusion for 90 min and then treated with or without 2% isoflurane for 60 min started at the onset of reperfusion. The infarct volumes, neurologic deficit scores, and performance on rotarod were evaluated at 24 h after the onset of reperfusion. Results Isoflurane applied immediately after the 15-min OGD for 30 min dose-dependently reversed the OGD-induced decrease of TTC conversion. The TTC conversion was 34 +/- 16% and 58 +/- 28% of the control, respectively, for OGD alone and OGD plus 2% isoflurane (P &lt; 0.05, n = 12). Application of 2% isoflurane for 30 min started at 10 min after the OGD also reduced the OGD-decreased TTC conversion. The presence of 0.3 microm glibenclamide, a general adenosine 5'-triphosphate-sensitive potassium channel blocker, or 500 microm 5-hydroxydecanoic acid, a mitochondrial adenosine 5'-triphosphate-sensitive potassium channel blocker, during the application of 2% isoflurane abolished the isoflurane preservation of TTC conversion. Application of isoflurane during reperfusion also improved neurologic outcome after brain ischemia. Conclusions The results suggest that isoflurane administrated after OGD or brain ischemia provides neuroprotection. Mitochondrial adenosine 5'-triphosphate-sensitive potassium channels may be involved in this protection.

scholarly journals Neurological manifestations of malaria

1992 ◽  
Vol 50 (1) ◽  
pp. 03-09 ◽  
Author(s):  
Gustavo C. Román ◽  
Nimal Senanayake
Keyword(s):  
Cerebral Malaria ◽  
Inflammatory Responses ◽  
Arterial Occlusion ◽  
Later Life ◽  
Endothelial Damage ◽  
Periodic Paralysis ◽  
Neurological Manifestations ◽  
Immunological Mechanisms ◽  
Peripheral Nerve Involvement ◽  
Cerebral Arterial Occlusion

The involvement of the nervous system in malaria is reviewed in this paper. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red cells causing sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes nonspecific, immune-mediated, inflammatory responses with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations remains unexplored, but offers excellent perspectives for research at a clinical as well as experimental level.

ADAMTS13 Gene Deletion Aggravates Ischemic Brain Damage

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 260-260 ◽  
Author(s):  
Kenji Nishio ◽  
Masayuki Fujioka ◽  
Kazuhide Hayakawa ◽  
Kenichi Mishima ◽  
Michihiro Fujiwara ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Arterial Occlusion ◽  
Neurological Deficits ◽  
Doppler Flowmetry ◽  
Adamts13 Deficiency ◽  
Cerebral Arterial Occlusion ◽  
The Brain

Abstract Background: The proteolytic activity of human ADAMTS13 regulates the size of von Willebrand factor (VWF) multimers, controlling excessive platelet aggregation and preventing microvascular thrombus formation. Deficiency of ADAMTS13 causes thrombotic thrombocytopenic purpura (TTP) and patients with TTP often have neurological deficits such as stupor or coma. Therefore, ADAMTS13 appears necessary for vascular homeostasis in the brain and may also influence the response to brain injury during ischemic stroke. Method and Result: We investigated the role of ADAMTS13 in a mouse middle cerebral arterial occlusion (MCAO) model of ischemia-reperfusion injury in the brain. We compared 24 wild type mice (WT) and 24 ADAMTS13 gene deleted mice (KO), which are healthy and fertile. All mice were males 6–8 weeks of age. Investigators were blinded to the genotype until all analyses were finished. We applied MCAO for 30 minutes followed by 23.5 hours of reperfusion. The cerebral blood flow (CBF) around the cortex of the ischemic region was measured by laser Doppler flowmetry for 60 minutes after MCAO. In both WT and KO mice, the CBF decreased to less than 20% of baseline during MCAO and returned to normal immediately after reperfusion. However, during the subsequent 30 min the CBF decreased to 34.6±5.8% of baseline for KO mice compared to 83.2±6.8% of baseline for WT mice (P &lt; 0.01) and remained significantly decreased at 24 hours, suggesting that ADAMTS13 deficiency promotes thrombosis after reperfusion injury. The infarction volumes of the brain were determined from the area not stained by 2,3,5,-triphenyltetrazolium chloride (TTC) 24 hours after MCAO. KO mice had significantly increased volume of brain infarction compared with WT (31.0±6.5mm3 vs 11.4±1.9 mm3, P &lt; 0.01). The degree of post-ischemic inflammation was estimated by Western blotting of plasma HMGB1 (high-mobility group box1) 24 hours after MCAO. Plasma HMGB1 was increased to 34.4 ± 5.3 ng/ml in KO mice, compared to 19.6 ± 3.5 ng/ml in WT mice (P &lt; 0.05). The KO and WT mice did not differ during the MCAO procedure in body temperature, survival (80% vs 85%) at 24 hours, prothrombin time, arterial pH, pO2 or pCO2. Conclusion: ADAMTS13 deficiency aggravates the extent of persistent brain ischemia, infarct volume and inflammatory response after brief MCAO. Therefore, ADAMTS13 plays a neuroprotective role against ischemia-reperfusion injury.

Sign in / Sign up

Export Citation Format

Share Document