scholarly journals Biphasic Opening of the Blood-Brain Barrier Following Transient Focal Ischemia: Effects of Hypothermia

1999 ◽  
Vol 26 (4) ◽  
pp. 298-304 ◽  
Author(s):  
Z. Gao Huang ◽  
Dong Xue ◽  
Hasneen Karbalai ◽  
Alastair M. Buchan ◽  
Z. Gao Huang ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Blood Brain Barrier ◽  
Cerebral Artery ◽  
Focal Ischemia ◽  
Brain Barrier ◽  
Whole Body ◽  
Second Phase ◽  
Blood Brain ◽  
The Right ◽  
Time Point

Objective:Tracer constants (Ki) for blood-to-brain diffusion of sucrose were measured in the rat to profile the time course of blood-brain barrier injury after temporary focal ischemia, and to determine the influence of post-ischemic hypothermia.Methods:Spontaneously hypertensive rats were subjected to transient (2 hours) clip occlusion of the right middle cerebral artery. Reperfusion times ranged from 1.5 min to 46 hours, and i.v. 3H-sucrose was circulated for 30 min prior to each time point (1h, 4h, 22h, and 46h; n=5-7 per time point). Ki was calculated from the ratio of parenchymal tracer uptake and the time-integrated plasma concentration. Additional groups of rats (n=7-8) were maintained either normothermic (37.5oC) or hypothermic (32.5oC or 28.5oC) for the first 6 hours of reperfusion, and Ki was measured at 46 hours.Results:Rats injected after 1.5 - 2 min exhibited a 10-fold increase in Ki for cortical regions supplied by the right middle cerebral artery (p<0.01). This barrier opening had closed within 1 to 4 hours post-reperfusion. By 22 hours, the blood-brain barrier had re-opened, with further opening 22 and 46 hours (p<0.01), resulting in edema. Whole body hypothermia (28oC-29oC) during the first six hours of reperfusion prevented opening, reducing Ki by over 50% (p<0.05).Conclusion:Transient middle cerebral artery occlusion evokes a marked biphasic opening of the cortical blood-brain barrier, the second phase of which causes vasogenic edema. Hypothermic treatment reduced infarct volume and the late opening of the blood-brain barrier. This opening of the blood-brain barrier may enhance delivery of low permeability neuroprotective agents.

scholarly journals Detrimental role of pericyte Nox4 in the acute phase of brain ischemia

2015 ◽  
Vol 36 (6) ◽  
pp. 1143-1154 ◽  
Author(s):  
Ataru Nishimura ◽  
Tetsuro Ago ◽  
Junya Kuroda ◽  
Koichi Arimura ◽  
Masaki Tachibana ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Blood Brain Barrier ◽  
Cerebral Artery ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Brain Barrier ◽  
Blood Brain ◽  
Barrier Breakdown ◽  
Cerebral Artery Occlusion

Pericytes are mural cells abundantly present in cerebral microvessels and play important roles, including the formation and maintenance of the blood–brain barrier. Nox4 is a major source of reactive oxygen species in cardiovascular cells and modulate cellular functions, particularly under pathological conditions. In the present study, we found that the expression of Nox4 was markedly induced in microvascular cells, including pericytes, in peri-infarct areas after middle cerebral artery occlusion stroke models in mice. The upregulation of Nox4 was greater in a permanent middle cerebral artery occlusion model compared with an ischemia/reperfusion transient middle cerebral artery occlusion model. We performed permanent middle cerebral artery occlusion on mice with Nox4 overexpression in pericytes (Tg-Nox4). Infarct volume was significantly greater with enhanced reactive oxygen species production and blood–brain barrier breakdown in peri-infarct areas in Tg-Nox4, compared with littermate controls. In cultured brain pericytes, Nox4 was significantly upregulated by hypoxia and was promptly downregulated by reoxygenation. Phosphorylation of NFκB and production of matrix metalloproteinase 9 were significantly increased in both cultured pericytes overexpressing Nox4 and in peri-infarct areas in Tg-Nox4. Collectively, Nox4 is upregulated in pericytes in peri-infarct areas after acute brain ischemia and may enhance blood–brain barrier breakdown through activation of NFκB and matrix metalloproteinase 9, thereby causing enlargement of infarct volume.

scholarly journals Verapamil-induced breakdown of the blood–brain barrier presenting as a transient right middle cerebral artery syndrome

2017 ◽  
Vol 23 (6) ◽  
pp. 601-604 ◽  
Author(s):  
Jonathan Pace ◽  
Jeffrey Nelson ◽  
Abhishek Ray ◽  
Yin Hu
Keyword(s):  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Middle Cerebral Artery ◽  
Blood Brain Barrier ◽  
Cerebral Artery ◽  
Internal Carotid ◽  
Right Hemisphere ◽  
Brain Barrier ◽  
Left Internal Carotid Artery ◽  
Blood Brain

A middle-aged patient presented for elective embolization of an incidentally found right internal carotid aneurysm. An angiogram was performed, during which the left internal carotid artery was visualized to evaluate a second, small aneurysm. During the embolization of the right internal carotid artery aneurysm, a catheter-induced vasospasm was identified that prompted treatment with intra-arterial verapamil. The procedure was uncomplicated; a postoperative rotational flat-panel computed tomography scan was performed on the angiography table that demonstrated right hemisphere contrast staining. The patient developed a right middle cerebral artery (MCA) syndrome after extubation with repeat cerebral angiography negative for occlusion and magnetic resonance imaging negative for stroke. The patient was observed for 48 hours, during which time the patient had slowly improved. At a six-week follow up visit, the patient had fully recovered. We present an interesting case of a verapamil-induced breakdown of the blood–brain barrier and self-limited right MCA syndrome.

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