scholarly journals DECOMPRESSIVE CRANIOTOMY IN MANAGEMENT OF ACUTE CEREBRAL ISCHEMIA

2021 ◽  
Vol 50 (4) ◽  
pp. 2565-2574
Keyword(s):  
Cerebral Ischemia ◽  
Decompressive Craniotomy ◽  
Acute Cerebral Ischemia

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.

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

Influence of Differences in Case Mix on the Better Outcome of Smokers after Intravenous Thrombolysis for Acute Cerebral Ischemia

2012 ◽  
Vol 67 (3) ◽  
pp. 178-183 ◽  
Author(s):  
Solène Moulin ◽  
Visnja Padjen-Bogosavljevic ◽  
Aurélie Marichal ◽  
Charlotte Cordonnier ◽  
Dejana R. Jovanovic ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Intravenous Thrombolysis ◽  
Case Mix ◽  
Acute Cerebral Ischemia

MRI of spontaneous fluctuations after acute cerebral ischemia in nonhuman primates

2007 ◽  
Vol 26 (4) ◽  
pp. 1112-1116 ◽  
Author(s):  
Yutong Liu ◽  
Helen D'Arceuil ◽  
Julian He ◽  
Mike Duggan ◽  
Gilberto Gonzalez ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nonhuman Primates ◽  
Acute Cerebral Ischemia ◽  
Spontaneous Fluctuations

Activation of complement by tissue plasminogen activator, but not acute cerebral ischemia, in a rabbit model of thromboembolic stroke

1997 ◽  
Vol 86 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Martin M. Bednar ◽  
Cordell E. Gross ◽  
Sheila R. Russell ◽  
David Short ◽  
Patricia C. Giclas
Keyword(s):  
Cerebral Ischemia ◽  
Plasminogen Activator ◽  
Complement Activation ◽  
Rabbit Model ◽  
Thromboembolic Stroke ◽  
Content Type ◽  
Acute Cerebral Ischemia ◽  
Tissue Plasminogen ◽  
Before And After ◽  
Fine Print

✓ Although complement activation is associated with tissue injury during inflammatory and ischemic states, complement activation in states of acute cerebral ischemia before and after administration of tissue plasminogen activator (TPA) has not yet been examined and is the focus of this investigation. Twenty-four New Zealand White rabbits weighing 3 to 3.5 kg were used for this study. Of these, 20 were subjected to intracranial autologous clot embolization via the internal carotid artery. Three hours postembolization, rabbits received an intravenous infusion of TPA (6.3 mg/kg, 20% bolus with the remainder infused over a 2-hour interval; 12 animals) or vehicle (eight animals). All animals were observed for a total of 7 or 8 hours postembolization. These two groups were compared to a cohort undergoing sham operation with subsequent TPA infusion (four animals). Plasma samples to quantify complement component C5 hemolytic activity (C5H5O) were obtained at the following time points: 30 minutes before and after clot embolization; 1 hour before and 1 hour after the initiation of therapy with TPA or vehicle and at the completion of the protocol; 7 to 8 hours after clot embolization. The C5 activation was not detected as the result of acute cerebral ischemia. However, animals receiving TPA with or without concomitant clot embolization exhibited C5 activation as assessed by a reduction in C5 hemolytic function, both 1 hour after initiation of TPA infusion (78.7 ± 10.3% and 77.5 ± 9.9% of baseline value, respectively; mean ± standard error of the mean [SEM]) and at the end of the protocol, 2 hours after the completion of the TPA infusion (72.5 ± 8.8% and 53.3 ± 8.1%, respectively; mean ± SEM, p < 0.05, each group). This study supports the conclusion that TPA, but not acute cerebral ischemia, may activate the complement cascade in this rabbit model of thromboembolic stroke.

scholarly journals Upregulation of CD40-CD40 Ligand (CD154) in Patients With Acute Cerebral Ischemia

Stroke ◽  
2003 ◽  
Vol 34 (6) ◽  
pp. 1412-1418 ◽  
Author(s):  
C.D. Garlichs ◽  
S. Kozina ◽  
S. Fateh-Moghadam ◽  
B. Tomandl ◽  
C. Stumpf ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Cd40 Ligand ◽  
Acute Cerebral Ischemia

Abstract TMP90: Frequency and Risk Factors for Early Neurological Deterioration Among Hyperacute Cerebral Ischemia Patients Treated With and Without Thrombolysis

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Christa D Brown ◽  
Gilda Avila-Rinek ◽  
Nerses Sanossian ◽  
Sidney Starkman ◽  
Scott Hamilton ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cerebral Ischemia ◽  
Fold Increase ◽  
Information Criteria ◽  
Neurological Deterioration ◽  
Stroke Severity ◽  
Acute Cerebral Ischemia ◽  
Early Neurological Deterioration ◽  
Prior Stroke ◽  
Iv Tpa

Background: Early neurological deterioration (END) is a feared complication of acute cerebral ischemia. However, estimates of END frequency vary widely, rates have not been systematically examined in hyperacute patients presenting within the first 2h of onset, nor separately in patients treated with and without thrombolysis, and risk factors for END have not been well delineated. Methods: We analyzed patients with a final diagnosis of acute cerebral ischemia in the NIH FAST-MAG Phase 3 multicenter clinical trial. END was defined as worsening post-admission by ≥ 4 NIHSS points up to Day 4. We separately analyzed patients who did and did not receive IV tPA. Results: Among 1245 acute cerebral ischemia patients transported by EMS to 55 stroke centers, time from last known well (LKW) to ED arrival was median 59 mins (IQR 80-46), and 36.1% received IV tPA. Overall, 211 (16.9%) experienced END by Day 4, with a greater proportion of END in tPA than non-tPA patients (21.2% vs 14.5%, p=0.003). In multivariate analysis, from 26 candidate variables, among tPA recipients, independent predictors of END were: age (OR 1.03/year, 95%CI 1.01-1.05), diastolic BP (OR 1.01/mm Hg, 95%CI 1.00-1.03), prior stroke (OR 1.65, 95%CI 0.98-2.77), glucose (OR 11.06/10 fold increase, 95%CI 1.90-64.44), and worse ASPECTS score (OR 0.85/point, 95%CI 0.78-0.92). Among non-tPA recipients, independent predictors of END were: more severe NIHSS (OR 1.08/point, 95%CI 1.05-1.11), glucose (OR 8.88/10 fold increase, 95%CI 1.83-43.12), and h/o hypertension (OR 2.62/mm Hg, 95%CI 1.25-5.48), with Akaike information criteria identifying SBP, shorter LKW-to-ED time, and absence of anticoagulant agents as additional contributors. C statistics for these models were 0.68 for tPA patients and 0.73 for non-tPA patients. Conclusions: Among hyperacute cerebral ischemia patients, END occurs in 1 in 5 who receive tPA, and 1 in 7 who do not receive tPA. Greater initial stroke severity (on neurologic exam or imaging), higher glucose, and hypertension increase risk of END for both lytic and non-lytic patients, with older age and prior stroke additionally increasing END risk with tPA. Models based on these risk factors show fair to good performance identifying patients who will experience END after hospital admission.

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