scholarly journals Protective effect of Fluosol-DA in acute cerebral ischemia.

Stroke ◽  
1981 ◽  
Vol 12 (5) ◽  
pp. 558-563 ◽  
Author(s):  
S J Peerless ◽  
R Ishikawa ◽  
I G Hunter ◽  
M J Peerless
Keyword(s):  
Cerebral Ischemia ◽  
Protective Effect ◽  
Acute Cerebral Ischemia

scholarly journals Protective effect of grifolin against brain injury in an acute cerebral ischemia rat model

2017 ◽  
Vol 16 (6) ◽  
pp. 1299 ◽  
Author(s):  
Shan Jing ◽  
Piaopiao Ying ◽  
Xiaohua Hu ◽  
Ze Yu ◽  
Jianwei Sun ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Protective Effect ◽  
Rat Model ◽  
Acute Cerebral Ischemia

Protective Effect of Paeoniflorin on Acute Cerebral Infarction in Rats

2020 ◽  
Vol 21 (8) ◽  
pp. 702-709
Author(s):  
Weilin Wu ◽  
Chenfeng Qiu ◽  
Xuewen Feng ◽  
Xiaoxiao Tao ◽  
Qian Zhu ◽  
...  
Keyword(s):  
Lactate Dehydrogenase ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Protective Effect ◽  
Brain Tissue ◽  
Cell Damage ◽  
Acute Cerebral Infarction ◽  
Neurological Deficits ◽  
Sod Activity ◽  
Acute Cerebral Ischemia

Objective: The purpose of this paper was to study the protective effect of paeoniflorin on acute cerebral ischemia. The animal model of cerebral infarction induced by Middle Cerebral Artery Occlusion (MCAO) was blocked by the suture method. Sixty SD rats were randomly divided into the shame group, MCAO group, paeoniflorin (60, 120, 240 mg/kg, respectively) and Nimodipine (NMDP) group (n = 10 per group). Methods: The rats were intragastrically administered immediately after the operation. After 7 days of gavage, the brains were decapitated at 24 h. Hematoxylin and Eosin (HE) staining was used to observe the degree of cell damage in the cerebral cortex of rats. Immunohistochemistry was used to detect silver plating and to observe changes in nerve cells. Rats in the model group showed obvious symptoms of neurological deficits, such as the ischemic morphological changed, the Malondialdehyde (MDA), Lactate Dehydrogenase (LD) content and lactate dehydrogenase (LDH) activity were significantly increased in the ischemic brain tissue, while the Superoxide Dismutase (SOD) activity was decreased. Results: The decrease in Na+-K+-ATPase activity was significantly lower than that in the sham group. The neurological symptoms and signs of MCAO in the different doses of paeoniflorin group were improved, and the neuronal edema in the cortical area was alleviated. The activities of SOD, LDH and Na+-K+-ATPase were significantly increased, and the contents of MDA and LD were decreased. Conclusion: Therefore, paeoniflorin could alleviate the degree of tissue damage in rats with acute cerebral infarction, inhabit the formation of free radicals in the brain tissue after ischemia, and reduce the degree of lipid peroxidation. Thus, the degree of cell damage was reduced greatly and a protective effect was showed on cerebral ischemia.

The protective effect of lipophilic iron chelator 2, 2′-dipyridyl after focal cerebral ischemia closely correlates with limitation of apoptotic cell death

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S482-S482
Author(s):  
Michaël C Van Hoecke ◽  
Anne Prigent-Tessier ◽  
Philippe E Garnier ◽  
Christine Marie ◽  
Alain Beley
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Protective Effect ◽  
Apoptotic Cell ◽  
Focal Cerebral Ischemia ◽  
Iron Chelator ◽  
Apoptotic Cell Death

Effect of carvedilol on the redox-status of plasma low-molecular-weight aminothyols in rats with acute cerebral ischemia

2018 ◽  
pp. 12-18
Author(s):  
К.А. Никифорова ◽  
В.В. Александрин ◽  
П.О. Булгакова ◽  
А.В. Иванов ◽  
Э.Д. Вирюс ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Cerebral Ischemia ◽  
Carotid Arteries ◽  
Redox Status ◽  
Global Cerebral Ischemia ◽  
Low Molecular Weight ◽  
Adrenergic Antagonist ◽  
Acute Cerebral Ischemia ◽  
Common Carotid Arteries ◽  
Reduced Forms

Цель. Установить влияние неспецифического адреноблокатора карведилола на редокс-статус низкомолекулярных аминотиолов (цистеин, гомоцистеин, глутатион) в плазме крови при моделировании глобальной ишемии головного мозга у крыс. Методика. Нами была использована модель глобальной ишемии (пережатие общих сонных артерий с геморрагией длительностью 15 мин). Препарат вводили за 1 ч до операции. Уровни аминотиолов измеряли через 40 мин после начала реперфузии. Анализ уровня аминотиолов проводили методом жидкостной хроматографии. Результаты. Установлено, что у крыс, не подвергавшихся ишемии, карведилол в дозе 10 мг/кг вызывает рост редокс-статуса цистеина и глутатиона (в 3 и 3,5 раза соответственно по сравнению с контролем, p = 0,04 и p = 0,008) за счет увеличения их восстановленных форм. При ишемии данного эффекта не наблюдалось. Редокс-статус у крыс с ишемией на фоне карведилола (Цис = 0,85 ± 0,14%, Глн = 1,8 ± 0,7%, Гцис = 1,1 ± 0,8%) оставался таким же низким, как и у крыс с ишемией без введения карведилола (р > 0,8). Заключение. Полученный результат демонстрирует, что в условиях ишемии головного мозга карведилол не оказывает эффекта на гомеостаз аминотиолов плазмы крови, несмотря на выраженный антиоксидантный эффект в нормальных условиях. Aim. Effect of a nonspecific adrenergic antagonist carvedilol on the redox status of plasma low-molecular-weight aminothiols (cysteine, homocysteine, glutathione) was studied in rats with global cerebral ischemia (occlusion of common carotid arteries with hemorrhage). Methods. A model of global ischemia (occlusion of common carotid arteries with 15-min hemorrhage) was used. The drugs were administered one hour before the operation. Aminothiol levels were measured by HPLC with UV detection at 40 minutes after the onset of reperfusion. Results. Carvedilol 10 mg/kg increased the redox status of cysteine and glutathione in rats not exposed to ischemia (3 and 3.5 times, respectively, compared with the control, p = 0.04 and p = 0.008, respectively) but not of homocysteine, by increasing their reduced forms. However, this effect was not observed in ischemia. In rats with ischemia treated with carvedilol, the redox status (Cys = 0.85 ± 0.14%, GSH = 1.8 ± 0.7%, Hcys = 1.1 ± 0.8%) remained low similar to that in rats with ischemia not treated with carvedilol (p >0.8, 0.8, and 0.9, respectively). Conclusion. Carvedilol did not affect the homeostasis of blood plasma thiols in cerebral ischemia despite the pronounced antioxidant effect under the normal conditions.

Losartan alleviates acute cerebral ischemia in spontaneously hypertensive rats:the arterial baroreflex function

2009 ◽  
Vol 29 (10) ◽  
pp. 1126-1130
Author(s):  
Jian WU ◽  
Rui-rui ZHOU ◽  
Jin-min GUO ◽  
Guo-jun CAI ◽  
Ai-jun LIU ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Arterial Baroreflex ◽  
Spontaneously Hypertensive ◽  
Baroreflex Function ◽  
Acute Cerebral Ischemia

scholarly journals A dose-escalation study of large doses of naloxone for treatment of patients with acute cerebral ischemia.

Stroke ◽  
1986 ◽  
Vol 17 (3) ◽  
pp. 404-409 ◽  
Author(s):  
H P Adams ◽  
C P Olinger ◽  
W G Barsan ◽  
M J Butler ◽  
N R Graff-Radford ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Dose Escalation ◽  
Dose Escalation Study ◽  
Acute Cerebral Ischemia
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