scholarly journals A Recombinant Inhibitory Isoform of Vascular Endothelial Growth Factor164/165 Aggravates Ischemic Brain Damage in a Mouse Model of Focal Cerebral Ischemia

2013 ◽  
Vol 183 (3) ◽  
pp. 1010-1024 ◽  
Author(s):  
Ganta V. Chaitanya ◽  
Walter E. Cromer ◽  
Courtney P. Parker ◽  
Pierre O. Couraud ◽  
Ignacio A. Romero ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Mouse Model ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Vascular Endothelial ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

scholarly journals Characteristics of nervous tissue after modeling of focal cerebral ischemia in rats at different periods of reperfusion

2018 ◽  
Vol 24 (3) ◽  
pp. 58-64
Author(s):  
O.I. Savchuk ◽  
G.G. Skibo
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Nervous Tissue ◽  
Focal Cerebral Ischemia ◽  
Tactile Sensitivity ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Ischemic Period ◽  
The Brain ◽  
Occlusion Period

The stroke-causing problems are extremely important in Ukraine. This makes a heavy burden not only on the health care system, but also on the whole society as a whole. That's why we've studied structural and ultrastructural changes of cortical neurons and striatum of the brain and the development of delayed death of nerve cells after the modeling of the middle cerebral artery occlusion (MCAO) and post ischemic period in rats. We've analyzed the data at different terms after modeling of MCAO. The purpose of the study was to investigate the changes in the nervous tissue in the modeling of focal cerebral ischemia by monofilament occlusion of MCAO in rats at different periods of reperfusion. The statistical processing of primary digital experimental data was carried out using the software Statistica 6.0. It was confirmed that the 60-minute occlusion of the MCAO is an adequate model of focal ischemic brain damage in rats. Changes of locomotor activity and a tactile sensitivity were determined in rats after occlusion and after reperfusion during the post-period period. It was found that in the experimental group with a reperfusion period of 72 hours, a clear increase of the volume of the ischemic area of the brain, accompanied by significant neurological deficiency, was observed. Reduced research activity of the rats was revealed, which was shown in the decrease of the number of squares they crossed, the number of racks, the increase of acts of grooming and the duration of acts of frizings. Following ischemic brain damage, there was also a disbalance of somato-sensory functions, as evidenced by an increase in the time during which the animal took a test stimulus ("Sticky tape") from both the anterior paws when tested for tactile sensitivity (adhesive removal test). An electron microscopic study of the cortex showed that dark wrinkled neurons and enlightened swollen neurons were observed at 72 hours of post-occlusion period, indicating different ways of death of these cells. Changes in striatum were similar to changes in the cortex, which progressed with an increase in the post-occlusion period. The protocol of the serial evaluation of neurological disorders used after MCAO modeling allowed detecting long-term stable functional disorders in laboratory rats. The obtained data indicate significant changes in the structure of the cortex and striatum in the post-ischemic period and the progressive nature of these changes.

scholarly journals Mito-Tempo prevents nicotine-induced exacerbation of ischemic brain damage

2018 ◽  
Vol 125 (1) ◽  
pp. 49-57 ◽  
Author(s):  
Chun Li ◽  
Hong Sun ◽  
Guodong Xu ◽  
Kimberly D. McCarter ◽  
Jiyu Li ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Neutrophil Infiltration ◽  
Neurological Deficits ◽  
Sprague Dawley ◽  
Ischemic Brain Damage ◽  
Mitochondrial Oxidative Stress ◽  
Ischemic Brain

Nicotine may contribute to the pathogenesis of cerebrovascular disease via the generation of reactive oxygen species (ROS). Overproduction of ROS leads to brain damage by intensifying postischemic inflammation. Our goal was to determine the effect of Mito-Tempo, a mitochondria-targeted antioxidant, on ischemic brain damage and postischemic inflammation during chronic exposure to nicotine. Male Sprague-Dawley rats were divided into four groups: control, nicotine, Mito-Tempo-treated control, and Mito-Tempo-treated nicotine. Nicotine (2 mg·kg−1·day−1) was administered via an osmotic minipump for 4 wk. Mito-Tempo (0.7 mg·kg−1·day−1ip) was given for 7 days before cerebral ischemia. Transient focal cerebral ischemia was induced by occlusion of the middle cerebral artery for 2 h. Brain damage and inflammation were evaluated after 24 h of reperfusion by measuring infarct volume, expression of adhesion molecules, activity of matrix metalloproteinase, brain edema, microglial activation, and neutrophil infiltration. Nicotine exacerbated infarct volume and worsened neurological deficits. Nicotine did not alter baseline ICAM-1 expression, matrix metallopeptidase-2 activity, microglia activation, or neutrophil infiltration but increased these parameters after cerebral ischemia. Mito-Tempo did not have an effect in control rats but prevented the chronic nicotine-induced augmentation of ischemic brain damage and postischemic inflammation. We suggest that nicotine increases brain damage following cerebral ischemia via an increase in mitochondrial oxidative stress, which, in turn, contributes to postischemic inflammation.NEW & NOTEWORTHY Our findings have important implications for the understanding of mechanisms contributing to increased susceptibility of the brain to damage in smokers and users of nicotine-containing tobacco products.

scholarly journals Protective Effect of the Glutamate Antagonist, MK-801 in Focal Cerebral Ischemia in the Cat

1988 ◽  
Vol 8 (1) ◽  
pp. 138-143 ◽  
Author(s):  
E. Ozyurt ◽  
D. I. Graham ◽  
G. N. Woodruff ◽  
J. McCulloch
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Middle Cerebral Artery ◽  
Brain Damage ◽  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Ischemic Damage ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Mk 801

The effects of the glutamate N-methyl-D aspartate (NMDA) receptor antagonist, MK-801, upon ischemic brain damage has been examined in anesthetized cats. Focal cerebral ischemia was produced by permanent occlusion of one middle cerebral artery and the animals were killed 6 h later. The amount of early ischemic damage was assessed in coronal sections at 16 predetermined stereotactic planes. Pretreatment with MK-801 (5 mg/kg, i.v.), 30 min before occlusion of the middle cerebral artery significantly reduced the volume of ischemic damage (from 32.7 ± 4.0% of the cerebral hemisphere in vehicle-treated cats to 16.2 ± 4.5% in MK-801-treated cats). NMDA receptor antagonists that penetrate the blood-brain barrier, such as MK-801, merit further study as protective agents against ischemic brain damage.

scholarly journals Focal Cerebral Ischemia in the Cat: Pretreatment with a Competitive NMDA Receptor Antagonist, D-CPP-ene

1990 ◽  
Vol 10 (5) ◽  
pp. 668-674 ◽  
Author(s):  
Ross Bullock ◽  
David I. Graham ◽  
Min-Hsiung Chen ◽  
David Lowe ◽  
James McCulloch
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Brain Damage ◽  
Cerebral Hemisphere ◽  
Focal Cerebral Ischemia ◽  
Nmda Receptor Antagonist ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Permanent Occlusion

The effects of the competitive N-methyl-D-aspartate (NMDA) receptor antagonist D-( E)-4-(3-phosphonoprop-2-enyl)piperazine-2-carboxylic acid (D-CPP-ene; SDZ EAA 494) upon ischemic brain damage have been examined in anesthetized cats. Focal cerebral ischemia was produced by permanent occlusion of the middle cerebral artery (MCA) and the animals were killed 6 h later. The amount of early ischemic brain damage was assessed in coronal sections at 16 predetermined stereotaxic planes. Pretreatment with D-CPP-ene (15 mg/kg i.v. followed by continuous infusion at 0.17 mg/kg/min until death), 15 min prior to MCA occlusion, significantly reduced the volume of ischemic brain damage (from 20.6 ± 9.9% of the cerebral hemisphere in vehicle-treated cats to 7.2 ± 4.4% in drug-treated cats; p < 0.01). The competitive NMDA receptor antagonist D-CPP-ene is as effective as noncompetitive NMDA antagonists in reducing the amount of ischemic brain damage in this model of focal cerebral ischemia in a gyrencephalic species.

Neuroprotective effect of tacrolimus (FK506) on ischemic brain damage following permanent focal cerebral ischemia in the rat

2004 ◽  
Vol 128 (1) ◽  
pp. 30-38 ◽  
Author(s):  
Takahisa Noto ◽  
Masayuki Ishiye ◽  
Yasuhisa Furuich ◽  
Yuriko Keida ◽  
Kiyotaka Katsuta ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

scholarly journals Continuous Nimodipine Treatment Attenuates Cortical Infarction in Rats Subjected to 24 Hours of Focal Cerebral Ischemia

1990 ◽  
Vol 10 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Michael Jacewicz ◽  
Steve Brint ◽  
Jody Tanabe ◽  
William A. Pulsinelli
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Spontaneously Hypertensive ◽  
Cortical Infarction ◽  
Cortical Edema ◽  
Tandem Occlusion

Focal cerebral infarction and edema were measured in rats (Wistar, Fisher 344, and spontaneously hypertensive strains) pretreated with nimodipine (2 μg/kg/min i.v.) or its vehicle and subjected to the tandem occlusion of the middle cerebral and common carotid arteries. Animals awoke from anesthesia 10–15 min after onset of ischemia and continued to receive treatment over a 24-h survival period. Cortical infarction and edema were quantified by image analysis of frozen brain sections processed for histology. Nimodipine-treated rats developed 20–60% smaller cortical infarct volumes than controls (p < 0.002). Cortical edema was reduced proportionately to the decrease in infarct volume and constituted ∼36% of the infarct volume. Nimodipine caused a mild hypotensive response that did not aggravate ischemic brain damage. The results indicate that continuous nimodipine treatment, started before induction of focal cerebral ischemia, can attenuate ischemic brain damage and edema as late as 24 h after the onset of ischemia.

Vasoactive intestinal peptide protects against ischemic brain damage induced by focal cerebral ischemia in rats

2011 ◽  
Vol 1398 ◽  
pp. 94-101 ◽  
Author(s):  
Jie Yang ◽  
Tian-Bao Song ◽  
Zhao-Hua Zhao ◽  
Shu-Dong Qiu ◽  
Xiao-Dan Hu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Vasoactive Intestinal Peptide ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Ischemic Brain Damage ◽  
Ischemic Brain
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