Tie2-expressing monocytes/macrophages promote cerebral revascularization in peri-infarct lesions upon ischemic insult

Maintaining a delicate balance among anticoagulant, procoagulant, and fibrinolytic pathways in the cerebral microcirculation is of major importance for normal cerebral blood flow. Under physiological conditions and in the absence of provocative stimuli, the anticoagulant and fibrinolytic pathways prevail over procoagulant mechanisms. Blood clotting is essential to minimize bleeding and to achieve hemostasis; however, excessive clotting contributes to thrombosis and may predispose the brain to infarction and ischemic stroke. Conversely, excessive bleeding due to enhanced anticoagulatory and fibrinolytic mechanisms could predispose the brain to hemorrhagic stroke. Recent studies in the author's laboratory indicate that brain capillary endothelium in vivo produces thrombomodulin (TM), a key cofactor in the TM-protein C system that is of major biological significance to the antithrombotic properties of the blood-brain barrier (BBB). The BBB endothelium also expresses tissue plasminogen activator (tPA), a key protein in fibrinolysis, and its rapid inhibitor, plasminogen activator inhibitor (PAI-1). The procoagulant tissue factor is normally dormant at the BBB. There is a vast body of clinical evidence to document the importance of hemostasis in the pathophysiology of brain injury. In particular, functional changes caused by major stroke risk factors in the TM-protein C, tPA/PAI-1, and tissue factor systems at the BBB may result in large and debilitating infarctions following an ischemic insult. Thus, correcting this hemostatic imbalance could ameliorate drastic CBF reductions at the time of ischemic insult, ultimately resulting in brain protection. Delineation of the molecular mechanisms of BBB-mediated hemostasis will likely contribute to future stroke prevention efforts and brain protection strategies.

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Acute Cerebral Revascularization Following Cerebral Embolism

Angiology ◽

10.1177/000331977903000604 ◽

1979 ◽

Vol 30 (6) ◽

pp. 407-415 ◽

Cited By ~ 16

Author(s):

Manuel Dujovny ◽

Ranjit K. Laha ◽

Pedro J. Barrionuevo ◽

Gonzalo Solis ◽

Guy Corkill

Keyword(s):

Cerebral Embolism ◽

Cerebral Revascularization

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Middle meningeal to middle cerebral arterial bypass for cerebral revascularization

Journal of Neurosurgery ◽

10.3171/jns.1979.50.6.0802 ◽

1979 ◽

Vol 50 (6) ◽

pp. 802-804 ◽

Cited By ~ 19

Author(s):

Clinton F. Miller ◽

Robert F. Spetzler ◽

Dennis J. Kopaniky

Keyword(s):

Middle Cerebral Artery ◽

Cerebral Artery ◽

Middle Meningeal Artery ◽

Cerebral Revascularization ◽

Content Type ◽

Arterial Bypass ◽

Meningeal Artery ◽

Fine Print

✓ A case is reported of successful anastomosis of the middle meningeal artery to a cortical branch of the middle cerebral artery. Based on the analyses of 50 random angiograms, the authors discuss the circumstances in which such an anastomosis might be practical and indicated.

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Quantitation of Photochemically Induced Focal Cerebral Ischemia in the Rat

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1988.11 ◽

1988 ◽

Vol 8 (1) ◽

pp. 89-95 ◽

Cited By ~ 77

Author(s):

John J. Grome ◽

Gerlinde Gojowczyk ◽

Wolfgang Hofmann ◽

David I. Graham

Keyword(s):

Cerebral Ischemia ◽

Water Content ◽

Rose Bengal ◽

Tissue Damage ◽

Focal Cerebral Ischemia ◽

Ischemic Damage ◽

Brain Water Content ◽

Ischemic Insult ◽

Ischemic Lesion ◽

Brain Water

This study was carried out with a recently developed model of focal cerebral ischemia in the rat based on the photochemical induction of thrombotic stroke using the dye Rose Bengal. We examined the change in the volume of the lesion and brain water content, in separate groups of rats, at different times (1, 4, 24, 72, and 168 h) after the induction of the ischemic lesion. The volume of ischemic damage increased rapidly between 1 and 24 h after the ischemic insult and decreased between 24 and 168 h. The lesion at 168 h was significantly larger than that following 1 h of ischemia and similar to that obtained at 4 h, suggesting that the maximum extent of tissue damage (without the involvement of significant edema) was reached within the first 4 h in this model. The enlargement of the lesion after 4 h correlated closely with changes in brain water content.

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Glucose Utilization in Rat Hippocampus after Long-Term Recovery from Ischemia

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1990.96 ◽

1990 ◽

Vol 10 (4) ◽

pp. 542-549 ◽

Cited By ~ 19

Author(s):

Thomas Beck ◽

Andreas Wree ◽

Axel Schleicher

Keyword(s):

Wistar Rats ◽

Carotid Arteries ◽

Glucose Utilization ◽

Pyramidal Cells ◽

Cresyl Violet ◽

Forebrain Ischemia ◽

Ischemic Insult ◽

Histological Damage ◽

Male Wistar Rats

The influence on hippocampal glucose utilization of a transient 10-min forebrain ischemia was quantified in male Wistar rats after 2 and 3 weeks as well as after 3 months by application of the [14C]2-deoxyglucose technique. Ischemia was induced by occlusion of the carotid arteries and simultaneous lowering of the blood pressure to 40 mm Hg. For identification of the hippocampal architecture, sections were stained for perikarya (cresyl violet) and for acetylcholinesterase. The hippocampal regions clearly showed different responses to the ischemic insult. The necrotic pyramidal cells being almost completely removed, significant increases in glucose utilization occurred in most layers of the CA1 sector at 2 and 3 weeks post ischemia, while widespread reductions prevailed in all other sectors and the dentate gyrus. At 3 months after the ischemic insult, glucose utilization was reduced in all hippocampal structures including the CA1 region. The increases in glucose utilization in the CA1 sector are suggested to indicate long-lasting presynaptic hyperexcitation, while the widespread reductions in glucose utilization demonstrate that neuronal activity is also altered in hippocampal areas that do not show major histological damage.

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Cerebral revascularization

Neurosurgery ◽

10.1097/00006123-197807000-00010 ◽

1978 ◽

Vol 3 (1) ◽

pp. 61???5 ◽

Cited By ~ 1

Author(s):

J L Story ◽

W E Brown ◽

E Eidelberg ◽

K V Arom ◽

J R Stewart

Keyword(s):

Cerebral Revascularization

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Treatment of aneurysms in patients with moyamoya disease: a 10-year single-center experience

Journal of Neurosurgery ◽

10.3171/2017.3.jns162290 ◽

2018 ◽

Vol 128 (6) ◽

pp. 1813-1822 ◽

Cited By ~ 6

Author(s):

Wei Ni ◽

Hanqiang Jiang ◽

Bin Xu ◽

Yu Lei ◽

Heng Yang ◽

...

Keyword(s):

Moyamoya Disease ◽

Posterior Circulation ◽

Cerebral Revascularization ◽

Endovascular Coiling ◽

Single Center ◽

Anterior Circulation ◽

Main Trunk ◽

Aneurysm Embolization ◽

Peripheral Aneurysms

OBJECTIVEMoyamoya disease (MMD) is occasionally accompanied by intracranial aneurysms. The purpose of this study was to delineate the efficacy of the authors’ current surgical strategy in the management of MMD-associated aneurysms of different types.METHODSBetween January 2007 and March 2016, a consecutive cohort of 34 patients with 36 MMD-associated aneurysms was enrolled in this prospective single-center cohort study. The lesions were classified as peripheral (17 aneurysms) or main trunk aneurysms (13 in the anterior circulation and 6 in the posterior circulation). For the peripheral aneurysms, revascularization with or without endovascular treatment was suggested. For the main trunk aneurysms, revascularization alone, revascularization with aneurysm clipping, or revascularization with aneurysm embolization were used, depending on the location of the aneurysms.RESULTSOf the peripheral aneurysms, 4 were treated endovascularly with staged revascularization, and 13 were treated solely with cerebral revascularization. Of the 13 main trunk aneurysms in the anterior circulation, 10 were clipped followed by revascularization, and 3 were coiled followed by staged cerebral revascularization. Of the 6 main trunk aneurysms in the posterior circulation, 4 underwent endovascular coiling and 2 were treated solely with revascularization. One patient died of contralateral intracerebral hemorrhage 6 months after the operation. No other patients suffered recurrent intracranial hemorrhage, cerebral ischemia, or aneurysm rupture. An angiographic follow-up study showed that all the bypass grafts were patent. Complete occlusion was achieved in all 21 aneurysms that were clipped or embolized. Of the remaining 15 aneurysms that were not directly treated, 12 of 13 peripheral aneurysms were obliterated during the follow-up, whereas 1 remained stable; 1 of 2 posterior main trunk aneurysms remained stable, and the other became smaller.CONCLUSIONSThe authors’ current treatment strategy may benefit patients with MMD-associated aneurysms.

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