Ovariectomy reduces vasocontractile responses of rat middle cerebral arteries after focal cerebral ischemia

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Mimmi Rehnström ◽  
Hilda Ahnstedt ◽  
Diana N. Krause ◽  
Marie Louise Edvinsson ◽  
Kristian Agmund Haanes ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Cerebral Arteries ◽  
Middle Cerebral Arteries

scholarly journals Regulatory Mechanism of Endothelin Receptor B in the Cerebral Arteries after Focal Cerebral Ischemia

PLoS ONE ◽  
2014 ◽  
Vol 9 (12) ◽  
pp. e113624 ◽  
Author(s):  
Anne-Sofie Grell ◽  
Rushani Thigarajah ◽  
Lars Edvinsson ◽  
Ajoy Kumar Samraj
Keyword(s):  
Cerebral Ischemia ◽  
Regulatory Mechanism ◽  
Focal Cerebral Ischemia ◽  
Cerebral Arteries ◽  
Endothelin Receptor ◽  
Endothelin Receptor B

scholarly journals Migraine and Ischemic Stroke: A Debated Question

2008 ◽  
Vol 28 (8) ◽  
pp. 1399-1421 ◽  
Author(s):  
Elisabetta Del Zotto ◽  
Alessandro Pezzini ◽  
Alessia Giossi ◽  
Irene Volonghi ◽  
Alessandro Padovani
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Causal Relation ◽  
Focal Cerebral Ischemia ◽  
Cerebral Arteries ◽  
Epidemiologic Studies ◽  
High Prevalence ◽  
Specific Disorders ◽  
New Research

Numerous epidemiologic observations reporting high prevalence of migraine among young individuals with stroke as well as dysfunction of cerebral arteries during migraine attacks prompt speculation on the existence of a comorbidity between the two disorders. The recent finding of silent infarct-like brain lesions in migraineurs reinforced this hypothesis and raised questions on whether migraine may be a progressive disorder rather than simply an episodic disorder. Stroke can occur during the course of migraine attacks with aura, supporting the assumption of a causal relation between the two diseases. Migraine may accentuate other existing risk factors for stroke, and both jointly increase the risk of cerebral ischemia outside of migraine attacks. In this regard, the role of migraine might be that of predisposing condition for cerebral ischemia. Migraine and ischemic stroke may be the end phenotype of common pathogenic mechanisms. Evidence of a migraine-stroke relation in cases of specific disorders, such as CADASIL (cerebral autosomal—dominant arteriopathy with subcortical infarcts and leukoencephalopathy) and MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes), strongly supports this concept. Finally, acute focal cerebral ischemia can trigger migraine attacks, and, thus, migraine may be the consequence of stroke. In this paper, we will review contemporary epidemiologic studies, discuss potential mechanisms of migraine-induced stroke and comorbid ischemic stroke, and pose new research questions.

scholarly journals Angiogenesis after Stroke is Correlated with Increased Numbers of Macrophages: The Clean-up Hypothesis

2001 ◽  
Vol 21 (10) ◽  
pp. 1223-1231 ◽  
Author(s):  
Panya S. Manoonkitiwongsa ◽  
Catherine Jackson-Friedman ◽  
Paul J. McMillan ◽  
Robert L. Schultz ◽  
Patrick D. Lyden
Keyword(s):  
Microvessel Density ◽  
Focal Cerebral Ischemia ◽  
Cerebral Arteries ◽  
Sprague Dawley ◽  
Regional Cerebral Blood ◽  
Ischemic Brain ◽  
Sprague Dawley Rats ◽  
Middle Cerebral Arteries ◽  
The Brain ◽  
Left Middle

Brain cells manufacture and secrete angiogenic peptides after focal cerebral ischemia, but the purpose of this angiogenic response is unknown. Because the maximum possible regional cerebral blood flow is determined by the quantity of microvessels in each unit volume, it is possible that angiogenic peptides are secreted to generate new collateral channels; other possibilities include neuroprotection, recovery/regeneration, and removal of necrotic debris. If the brain attempts to create new collaterals, microvessel density should increase significantly after ischemia. Conversely, if angiogenic-signaling molecules serve some other purpose, microvessel densities may increase slightly or not at all. To clarify, the authors measured microvessel densities with quantitative morphometry. Left middle cerebral arteries of adult male Sprague–Dawley rats were occluded with intraluminal nylon suture for 4 hours followed by 7, 14, 19, or 30 days of reperfusion. Controls received no surgery or suture occlusion. Changes in microvessel density and macrophage numbers were measured by light microscopic morphometry using semiautomated stereologic methods. Microvessel density increased only in the ischemic margin adjacent to areas of pannecrosis and was always associated with increased numbers of macrophages. Ischemic brain areas without macrophages displayed no vascularity changes compared with normal animals. These data suggest that ischemia-induced microvessels are formed to facilitate macrophage infiltration and removal of necrotic brain.

scholarly journals Peroxynitrite Formation in Focal Cerebral Ischemia—Reperfusion in Rats Occurs Predominantly in the Peri-Infarct Region

1998 ◽  
Vol 18 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Naoto Fukuyama ◽  
Shunya Takizawa ◽  
Hideyuki Ishida ◽  
Kiyotaka Hoshiai ◽  
Yukito Shinohara ◽  
...  
Keyword(s):  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Cerebral Arteries ◽  
Infarct Region ◽  
Tyrosine Residues ◽  
The Core ◽  
Middle Cerebral Arteries ◽  
The Right ◽  
Cellular Components ◽  
The Brain

Peroxynitrite (ONOO−) exhibits potent neurotoxicity and plays an important role in neu ronal death, but no evidence shows that it is formed in the brain during ischemia or subsequent reperfusion. To detect the formation of ONOO−, we used a hydrolysis/HPLC procedure to measure the formation of 3-nitro-l-tyrosine (NO2-Tyr), which is considered to reflect attack of ONOO− on l-tyrosine residues of cellular components in the brain. Focal ischemia was produced by occluding the right common carotid and right middle cerebral arteries for 2 hours, and the ischemic area was reperfused by reopening the middle cerebral artery. After 2 hours of ischemia, the values of the ratio of NO2-Tyr to l-tyrosine were 0% ± 0%, 0.42% ± 0.13% and 0.29% ± 0.10% in the noninfarct, periinfarct, and core-of-infarct regions, respectively. After 3 hours of reperfusion following 2 hours of ischemia, the ratio in the periinfarct region reached 0.89 ± 0.22%, which was significantly higher than that in the core-of-infarct region (0.35 ± 0.09%). The NO2-Tyr was not detected in 50 mg/kg of N-monomethyl-l-arginine–treated or sham-operated rats. Regional CBF in the periinfarct region decreased to 30.8 ± 15.9 mL/100 g/min during occlusion, but recovered more rapidly than did that in the core-of-infarct region.

scholarly journals The intracranial vasculature of canines represents a model for neurovascular ischemia and training residents and fellows in endovascular neurosurgery

2020 ◽  
Vol 33 (4) ◽  
pp. 292-296
Author(s):  
Xianli Lv ◽  
Chen Li ◽  
Weijian Jiang
Keyword(s):  
Cerebral Ischemia ◽  
Cerebral Arteries ◽  
Canine Model ◽  
Arteriovenous Fistulas ◽  
Middle Cerebral Arteries ◽  
Neuroprotective Strategies ◽  
Anesthetized Dogs ◽  
And Training ◽  
Intracranial Vasculature ◽  
Carotid And Vertebral Arteries

Background We describe use of a canine model to evaluate physiological effects and neuroprotective strategies in the setting of cerebral ischemia and endovascular neurosurgery training. Methods We performed transfemoral digital subtraction cerebral and cervical angiography on eight anesthetized dogs. Angiographic images of cerebral arteries were obtained following cannulation of the femoral artery. Cerebral ischemia models were made after angiography. Results The canine cerebral vasculature exhibited extensive tortuosity of the carotid and vertebral arteries. Conversely, the bilateral anterior spinal arteries were easily catheterized using microcatheters and microguidewires. The basilar artery and its branches were facilely cannulable. Circle of Willis continuity sans hypoplasia or aplasia of its constitutive segments was appreciated in all animals. The middle cerebral arteries could be easily accessed via the posterior communicating arteries. We generated an empirically evaluable therapeutically interventional experimental animal model of cerebral ischemia by occluding the middle cerebral artery using small coils for a duration between 15 and 60 min. Conclusion Unique amenability of the canine intracranial vasculature to selective and microcatheter cannulation renders experimentally induced cerebral, cerebellar, and brainstem via occlusion of the supratentorial and infratentorial arteries a simple matter. The neural vasculature irrigating the canine cerebrum, brainstem, and cerebellum may consequently prove useful in helping young and nascent endovascular neurosurgeons in developing and refining their skills of microcatheter navigation and manipulation and deployment of therapeutic devices to achieve effective occlusion of aneurysms, arteriovenous malformations, arteriovenous fistulas, and neoplasms of the intracranial cavity.

scholarly journals Selective Gene Expression in Focal Cerebral Ischemia

1986 ◽  
Vol 6 (3) ◽  
pp. 263-272 ◽  
Author(s):  
Michael Jacewicz ◽  
Marika Kiessling ◽  
William A. Pulsinelli
Keyword(s):  
Blood Flow ◽  
Protein Synthesis ◽  
Heat Shock ◽  
Focal Cerebral Ischemia ◽  
Cerebral Arteries ◽  
Regional Patterns ◽  
Ischemic Tissue ◽  
Middle Cerebral Arteries ◽  
The Right ◽  
Severe Ischemia

Regional patterns of protein synthesis were examined in rat cortex made ischemic by the occlusion of the right common carotid and middle cerebral arteries. At 2 h of ischemia, proteins were pulse labeled with intracortical injections of a mixture of [3H]leucine, [3H]isoleucine, and [3H]proline. Newly synthesized proteins were analyzed by two-dimensional gel fluorography, and the results correlated with local CBF, measured with [14C]iodoantipyrine as tracer. Small blood flow reductions (CBF = 50–80 ml 100 g−1 min−1) were accompanied by a modest inhibition in synthesis of many proteins and a marked increase in one protein (Mr 27,000). With further reduction in blood flow (CBF = 40 ml 100 g−1 min−1), synthesis became limited to a small group of proteins (Mr 27,000, 34,000, 73,000, 79,000, and actin) including two new polypeptides (Mr 55,000 and 70,000). Severe ischemia (CBF = 15–25 ml 100 g−1 min−1) caused the isoelectric modification of several proteins (Mr 44,000, 55,000, and 70,000) and induced synthesis of another protein (Mr 40,000). Two polypeptides (Mr 27,000 and 70,000) dominated residual protein synthesis in severe ischemia. The changes in protein synthesis induced by different grades of ischemia most likely comprise a variation of the so-called “heat shock” or “stress” response found in all eukaryotic cells subjected to adverse conditions. Since heat shock genes are known to confer partial protection against anoxia and a variety of other noxious insults, their induction may be a factor in limiting the extent of ischemic tissue damage.

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