Thrombin exacerbates brain edema in focal cerebral ischemia

2003 ◽  
pp. 163-166 ◽  
Author(s):  
Y. Hua ◽  
J. Wu ◽  
R. F. Keep ◽  
J. T. Hoff ◽  
Guohua Xi
Keyword(s):  
Cerebral Ischemia ◽  
Brain Edema ◽  
Focal Cerebral Ischemia

Nonhyperemic blood flow restoration and brain edema in experimental focal cerebral ischemia

1989 ◽  
Vol 70 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Toshihiko Kuroiwa ◽  
Makoto Shibutani ◽  
Riki Okeda
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Brain Edema ◽  
Focal Cerebral Ischemia ◽  
Reactive Hyperemia ◽  
Diffusion Method ◽  
Left Middle Cerebral Artery ◽  
Content Type ◽  
Bbb Opening ◽  
Fine Print

✓ The effect of suppression of postischemic reactive hyperemia on the blood-brain barrier (BBB) and ischemic brain edema after temporary focal cerebral ischemia was studied in cats under ketamine and alpha-chloralose anesthesia. Regional cerebral blood flow (rCBF) was measured by a thermal diffusion method and a hydrogen clearance method. The animals were separated into three groups. In Group A, the left middle cerebral artery (MCA) was occluded for 6 hours. In Group B, the MCA was occluded for 3 hours and then reperfused for 3 hours; postischemic hyperemia was suppressed to the preischemic level by regulating the degree of MCA constriction. In Group C, the MCA was occluded for 3 hours and reperfused for 3 hours without suppressing the postischemic reactive hyperemia. The brain was removed and cut coronally at the site of rCBF measurement. The degree of ischemic edema was assessed by gravimetry in samples taken from the coronal section and correlated with the degree of BBB disruption at the corresponding sites, evaluated by densitometric determination of Evans blue discoloration. The findings showed that 1) ischemic edema was significantly exacerbated by postischemic hyperemia during reperfusion in parallel with the degree of BBB opening to serum proteins, and 2) suppression of postischemic hyperemia significantly reduced the exacerbation of ischemic edema and BBB opening. These findings indicate that blood flow may be restored without significant exacerbation of postischemic edema by the suppression of postischemic hyperemia in focal cerebral ischemia.

Therapeutical efficacy of a novel non-peptide bradykinin B2 receptor antagonist on brain edema formation and ischemic tissue damage in focal cerebral ischemia

2003 ◽  
pp. 205-207 ◽  
Author(s):  
Stefan Zausinger ◽  
D. B. Lumenta ◽  
D. Pruneau ◽  
R. Schmid-Elsaesser ◽  
N. Plesnila ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Receptor Antagonist ◽  
Brain Edema ◽  
Tissue Damage ◽  
Focal Cerebral Ischemia ◽  
Edema Formation ◽  
Bradykinin B2 Receptor ◽  
Ischemic Tissue ◽  
Brain Edema Formation

Xanthine oxidase is not a major source of free radicals in focal cerebral ischemia

1991 ◽  
Vol 260 (2) ◽  
pp. H563-H568 ◽  
Author(s):  
A. L. Betz ◽  
J. Randall ◽  
D. Martz
Keyword(s):  
Uric Acid ◽  
Free Radicals ◽  
Cerebral Ischemia ◽  
Xanthine Oxidase ◽  
Brain Edema ◽  
Focal Cerebral Ischemia ◽  
Total Activity ◽  
Brain Regions ◽  
Free Radical Scavengers ◽  
Edema Formation

Xanthine oxidase (XO) has been proposed as an important source of free radicals during ischemia. This enzyme normally exists as a dehydrogenase (XD), but it is converted to XO in some ischemic tissues. Recently, treatment of animals with the XD and XO inhibitor allopurinol or with free radical scavengers before cerebral ischemia has been shown to reduce brain injury. Therefore, we studied conversion of XD to XO in three ischemic and nonischemic brain regions during focal cerebral ischemia resulting from permanent occlusion of the middle cerebral artery (MCAO) in anesthetized rats. In nonischemic brain, 16-22% of the enzyme was in the XO form. After 24 h of ischemia this value was not significantly different (10-15%). Neither the total activity of XO nor that of XD changed, indicating that there was no irreversible conversion of XD to XO. To further explore the possible role of XO, we examined the effect of various doses of allopurinol (5, 20, or 100 mg/kg given 1 h before MCAO or 100 mg/kg given 48, 24, and 1 h before MCAO) on uric acid accumulation, brain edema formation, and cerebral blood flow (CBF) 24 h after MCAO. All but the lowest dose of allopurinol greatly reduced the appearance of uric acid in the ischemic brain; however, only the highest dose of allopurinol had any beneficial effect on brain edema. This reduction in brain edema occurred without a significant improvement in CBF. Thus XO is probably not an important source of free radicals in this model of focal cerebral ischemia.

scholarly journals Nimodipine Pretreatment Improves Cerebral Blood Flow and Reduces Brain Edema in Conscious Rats Subjected to Focal Cerebral Ischemia

1990 ◽  
Vol 10 (6) ◽  
pp. 903-913 ◽  
Author(s):  
Michael Jacewicz ◽  
Steve Brint ◽  
Jody Tanabe ◽  
Xing-Je Wang ◽  
William A. Pulsinelli
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Brain Edema ◽  
Focal Cerebral Ischemia ◽  
Polyethylene Glycol 400 ◽  
Conscious Rats ◽  
Ischemic Core ◽  
Cortical Ischemia ◽  
Vascular Steal ◽  
Common Carotid Arteries

The effect of nimodipine pretreatment on CBF and brain edema was studied in conscious rats subjected to 2.5 h of focal cortical ischemia. An infusion of nimodipine (2 μg/kg/min i.v.) or its vehicle, polyethylene glycol 400, was begun 2 h before the ischemic interval and was continued throughout the survival period. Under brief halothane anesthesia, the animals' right middle cerebral and common carotid arteries were permanently occluded, and 2.5 h later, they underwent a quantitative CBF study ([14C]iodoantipyrine autoradiography followed by Quantimet 970 image analysis). Nimodipine treatment improved blood flow to the middle cerebral artery territory without evidence of a “vascular steal” and reduced the volume of the ischemic core (cortex with CBF of < 25 ml/100 g/min) and accompanying edema by ∼50% when compared with controls (p = 0.006 and 0.0004, respectively). Mild hypotension induced by nimodipine did not aggravate the ischemic insult. The ischemic core volumes, however, were 50–75% smaller than the 24-h infarct volumes generated in a similar paradigm that demonstrated 20–30% infarct reduction with continuous nimodipine treatment. These results suggest that nimodipine pretreatment attenuates the severity of early focal cerebral ischemia, but that with persistent ischemia, cortex surrounding the ischemic core undergoes progressive infarction and the early benefit of nimodipine treatment is only partly preserved.

Effect of aminoguanidine on post-ischemic brain edema in transient model of focal cerebral ischemia

2007 ◽  
Vol 1170 ◽  
pp. 97-102 ◽  
Author(s):  
Abedin Vakili ◽  
Fezzeh Hosseinzadeh ◽  
Toktam Sadogh
Keyword(s):  
Cerebral Ischemia ◽  
Brain Edema ◽  
Focal Cerebral Ischemia ◽  
Transient Model ◽  
Ischemic Brain ◽  
Ischemic Brain Edema

Delayed institution of hypertension during focal cerebral ischemia: effect on brain edema

1991 ◽  
Vol 81 (3) ◽  
pp. 339-344 ◽  
Author(s):  
P. M. Patel ◽  
J. C. Drummond ◽  
D. J. Cole ◽  
R. Giamela ◽  
J. Steinauer
Keyword(s):  
Cerebral Ischemia ◽  
Brain Edema ◽  
Focal Cerebral Ischemia

scholarly journals YiQiFuMai powder injection ameliorates blood–brain barrier dysfunction and brain edema after focal cerebral ischemia–reperfusion injury in mice

2016 ◽  
pp. 315 ◽  
Author(s):  
Junping Kou ◽  
Guosheng Cao ◽  
Xinyi Ye ◽  
Yingqiong Xu ◽  
Mingzhu Yin ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Brain Edema ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Powder Injection ◽  
Barrier Dysfunction

Role of Arginine Vasopressin V1 and V2 Receptors for Brain Damage After Transient Focal Cerebral Ischemia

2005 ◽  
Vol 25 (8) ◽  
pp. 1012-1019 ◽  
Author(s):  
Abedin Vakili ◽  
Hiroharu Kataoka ◽  
Nikolaus Plesnila
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Brain Edema ◽  
Brain Damage ◽  
Arginine Vasopressin ◽  
Focal Cerebral Ischemia ◽  
Edema Formation ◽  
Transient Focal Cerebral Ischemia ◽  
Brain Edema Formation

Brain edema formation is one of the most important mechanisms responsible for brain damage after ischemic stroke. Despite considerable efforts, no specific therapy is available yet. Arginine vasopressin (AVP) regulates cerebral water homeostasis and has been involved in brain edema formation. In the current study, we investigated the role of AVP V1 and V2 receptors on brain damage, brain edema formation, and functional outcome after transient focal cerebral ischemia, a condition comparable with that of stroke patients undergoing thrombolysis. C57/BL6 mice were subjected to 60-min middle cerebral artery occlusion (MCAO) followed by 23 h of reperfusion. Five minutes after MCAO, 100 or 500 ng of [deamino-Pen(1), O-Me-Tyr(2), Arg(8)]-vasopressin (AVP V1 receptor antagonist) or [adamantaneacetyl(1), O-Et-d-Tyr(2), Val(4), Abu(6), Arg(8,9)]-vasopressin (AVP V2 receptor antagonist) were injected into the left ventricle. Inhibition of AVP V1 receptors reduced infarct volume in a dose-dependent manner by 54% and 70% (to 29±13 and 19±10 mm3 versus 63±17 mm3 in controls; P<0.001), brain edema formation by 67% (to 80.4%±1.0% versus 82.7%±1.2% in controls; P<0.001), blood-brain barrier disruption by 75% ( P<0.001), and functional deficits 24 h after ischemia, while V2 receptor inhibition had no effect. The current findings indicate that AVP V1 but not V2 receptors are involved in the pathophysiology of secondary brain damage after focal cerebral ischemia. Although further studies are needed to clarify the mechanisms of neuroprotection, AVP V1 receptors seem to be promising targets for the treatment of ischemic stroke.

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