scholarly journals Worsened Outcome from Middle Cerebral Artery Occlusion in Aged Rats Receiving 17β-Estradiol

Endocrinology ◽  
2012 ◽  
Vol 153 (7) ◽  
pp. 3386-3393 ◽  
Author(s):  
Rachel L. Leon ◽  
Xinlan Li ◽  
Jason D. Huber ◽  
Charles L. Rosen
Keyword(s):  
Young Adult ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Female Rats ◽  
Aged Rats ◽  
Adult Rats ◽  
17Β Estradiol ◽  
Cerebral Artery Occlusion

Although estrogens are neuroprotective in young adult animal models of stroke, clinical trials demonstrate that estrogens increase the incidence and severity of stroke in aged women. We have previously shown that experimental stroke pathophysiology differs between young adult and aged rats. The aim of this study was to determine the effects of 17β-estradiol after middle cerebral artery occlusion and reperfusion in young adult and aged female rats. Focal embolic stroke was performed by middle cerebral artery occlusion with fibrin clot followed by reperfusion with iv human recombinant tissue plasminogen activator. Histological and functional outcomes were measured at 24 h after middle cerebral artery occlusion with fibrin clot. Aged rats treated with 17β-estradiol had significantly increased infarct volumes compared with placebo-treated aged rats. Young adult rats treated with 17β-estradiol had significantly decreased infarct volumes and improved functional outcome compared with ovariectomized young adult rats. Our results suggest that 17β-estradiol may act in an age-dependent manner in the postischemic rat brain. In young adult rats, it is neuroprotective; chronic treatment with 17β-estradiol during aging leads to worsened ischemic brain injury in aged female rats.

GABAergic contribution to rat bladder hyperactivity after middle cerebral artery occlusion

2000 ◽  
Vol 279 (4) ◽  
pp. R1230-R1238 ◽  
Author(s):  
Sayoko Kanie ◽  
Osamu Yokoyama ◽  
Kazuto Komatsu ◽  
Koichi Kodama ◽  
Satoshi Yotsuyanagi ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Receptor Agonist ◽  
Bladder Capacity ◽  
Artery Occlusion ◽  
Female Rats ◽  
Left Middle Cerebral Artery ◽  
Urethral Pressure ◽  
Cerebral Artery Occlusion

To evaluate the influences of γ-aminobutyric acid (GABA) mechanisms on bladder hyperactivity after left middle cerebral artery occlusion, cystometric recordings were obtained from unanesthetized female rats. Intracerebroventricular administration of both muscimol (GABAA receptor agonist; 0.1–10 nmol) and baclofen (GABAB receptor agonist; 0.1–3 nmol) produced dose-dependent inhibitions of micturition with increases in bladder capacity (BC). The effects of high doses (1–10 nmol) were similar in sham-operated (SO) and cerebral-infarcted (CI) rats. However, lower doses of muscimol (0.1 or 0.3 nmol) and baclofen (0.1 nmol) reduced BC in CI rats. After bicuculline (GABAA receptor antagonist; 1 or 3 nmol) administration, BC in both SO and CI rats first decreased and subsequently increased. An increase in urethral pressure was observed after administration of bicuculline (3 nmol) but not with either muscimol or baclofen. Infarct volumes in muscimol-, bicuculline-, or baclofen-treated rats were not significantly different from those of vehicle-treated rats. These results suggest that GABAergic mechanisms inhibit the micturition reflex at the supraspinal level but that this can change as a result of CI.

scholarly journals Bryostatin extends tPA time window to 6 h following middle cerebral artery occlusion in aged female rats

2015 ◽  
Vol 764 ◽  
pp. 404-412 ◽  
Author(s):  
Zhenjun Tan ◽  
Brandon P. Lucke-Wold ◽  
Aric F. Logsdon ◽  
Ryan C. Turner ◽  
Cong Tan ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Time Window ◽  
Artery Occlusion ◽  
Female Rats ◽  
Cerebral Artery Occlusion

scholarly journals Eyeballing stroke: Blood flow alterations in the eye and visual impairments following transient middle cerebral artery occlusion in adult rats

2020 ◽  
Vol 29 ◽  
pp. 096368972090580
Author(s):  
Jea-young Lee ◽  
Vanessa Castelli ◽  
Brooke Bonsack ◽  
Julián García-Sánchez ◽  
Chase Kingsbury ◽  
...  
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Laser Doppler ◽  
Adult Rats ◽  
Visual Deficits ◽  
Cerebral Artery Occlusion ◽  
The Brain

Middle cerebral artery occlusion in rodents remains a widely used model of ischemic stroke. Recently, we reported the occurrence of retinal ischemia in animals subjected to middle cerebral artery occlusion, owing in part to the circulatory juxtaposition of the ophthalmic artery to the middle cerebral artery. In this study, we examined the eye hemodynamics and visual deficits in middle cerebral artery occlusion-induced stroke rats. The brain and eye were evaluated by laser Doppler at baseline (prior to middle cerebral artery occlusion), during and after middle cerebral artery occlusion. Retinal function-relevant behavioral and histological outcomes were performed at 3 and 14 days post-middle cerebral artery occlusion. Laser Doppler revealed a typical reduction of at least 80% in the ipsilateral frontoparietal cortical area of the brain during middle cerebral artery occlusion compared to baseline, which returned to near-baseline levels during reperfusion. Retinal perfusion defects closely paralleled the timing of cerebral blood flow alterations in the acute stages of middle cerebral artery occlusion in adult rats, characterized by a significant blood flow defect in the ipsilateral eye with at least 90% reduction during middle cerebral artery occlusion compared to baseline, which was restored to near-baseline levels during reperfusion. Moreover, retinal ganglion cell density and optic nerve depth were significantly decreased in the ipsilateral eye. In addition, the stroke rats displayed eye closure. Behavioral performance in a light stimulus-mediated avoidance test was significantly impaired in middle cerebral artery occlusion rats compared to control animals. In view of visual deficits in stroke patients, closely monitoring of brain and retinal perfusion via laser Doppler measurements and examination of visual impairments may facilitate the diagnosis and the treatment of stroke, including retinal ischemia.

scholarly journals Cortical Neurogenesis in Adult Rats After Transient Middle Cerebral Artery Occlusion

Stroke ◽  
2001 ◽  
Vol 32 (5) ◽  
pp. 1201-1207 ◽  
Author(s):  
Wei Jiang ◽  
WeiGang Gu ◽  
Thomas Brännström ◽  
Roland Rosqvist ◽  
Per Wester
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Adult Rats ◽  
Cortical Neurogenesis ◽  
Cerebral Artery Occlusion

The effect of exercise preconditioning on stroke outcome in ovariectomized mice with permanent middle cerebral artery occlusion

2018 ◽  
Vol 96 (3) ◽  
pp. 287-294
Author(s):  
Soudabeh Naderi ◽  
Raheleh Alimohammadi ◽  
Elham Hakimizadeh ◽  
Ali Roohbakhsh ◽  
Ali Shamsizadeh ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Neurological Deficits ◽  
Stroke Outcome ◽  
Ovariectomized Mice ◽  
Exercise Preconditioning ◽  
17Β Estradiol ◽  
Cerebral Artery Occlusion

Exercise preconditioning has been shown to be effective in improving behavioral and neuropathological indices after cerebral ischemia. We evaluated the effect of exercise preconditioning, 17β-estradiol, and their combination on stroke outcome using an experimental model of stroke in ovariectomized (OVX) mice. OVX mice were randomly assigned to 4 groups as follows: control (stroke), exercise (exercise and stroke), estradiol (17β-estradiol and stroke), and exercise+estradiol (exercise and 17β-estradiol and stroke). Exercise preconditioning was performed on a treadmill 5 days/week, 40 min/day, at a speed of 18 m/min for 4 weeks. 17β-estradiol was gavaged (40 μg/kg per day) for 4 weeks. Stroke was induced by permanent middle cerebral artery occlusion (pMCAO), and neurological deficits were evaluated 1, 2, and 7 days after stroke. Then, the serum concentrations of matrix metalloproteinase-9 (MMP-9) and interleukin-10 (IL-10) and infarct volumes were assessed. Exercise preconditioning and 17β-estradiol induced a better outcome compared with the control ischemic mice, which was manifested by decrease in MMP-9, increase in IL-10, diminished infarct volume, and improved neurological deficits. Concomitant administration of 17β-estradiol and exercise also significantly improved these parameters. Exercise preconditioning or administration of 17β-estradiol alone or in combination before pMCAO induced significant neuroprotection in OVX mice.

scholarly journals Human C-Reactive Protein Increases Cerebral Infarct Size after Middle Cerebral Artery Occlusion in Adult Rats

2004 ◽  
Vol 24 (11) ◽  
pp. 1214-1218 ◽  
Author(s):  
Ramanjit Gill ◽  
John A. Kemp ◽  
Caroline Sabin ◽  
Mark B. Pepys
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
C Reactive Protein ◽  
Adult Rats ◽  
Reactive Protein ◽  
Cerebral Artery Occlusion

Human C-reactive protein (CRP), the classic acute phase plasma protein, increases in concentration after myocardial infarction and stroke. Human CRP binds to ligands exposed in damaged tissue and can then activate complement and its proinflammatory functions. In contrast, rat CRP, which binds to similar ligands, does not activate complement. In the present study, systemic complement depletion with cobra venom factor in adult rats subjected to middle cerebral artery occlusion did not affect cerebral infarct size, indicating that circulating complement does not contribute to injury in this model. However, we have previously reported that administration of human CRP to rats undergoing coronary artery ligation caused a marked increase in size of the resulting myocardial infarction, associated with codeposition of human CRP and rat complement in the infarcts. In the present study, we show that adult rats subjected to middle cerebral artery occlusion and then treated with human CRP similarly developed significantly larger cerebral infarcts compared with control subjects receiving human serum albumin. Human CRP can thus contribute to ischemic tissue damage in the brain as well as in the heart, and inhibition of CRP binding may therefore be a promising target for tissue protective acute therapeutic intervention in stroke as well as in myocardial infarction.

Sign in / Sign up

Export Citation Format

Share Document