Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We conducted a randomized, blinded controlled trial to test the efficacy of fibrinolytic therapy with tissue plasminogen activator and urokinase in the treatment of acute embolic stroke. Embolic stroke was simulated in rabbits by injecting three 0.5 x 0.5 mm fragments of autologous arterial thrombus harvested from a traumatized auricular artery. Thirty minutes after embolization the rabbits were blindly treated with tissue plasminogen activator (n = 21), urokinase (n = 20), or 0.9% saline (n = 20). At 6 hours the rabbits were sacrificed, and the cerebral vasculature was inspected for the location and number of emboli. The brain was then cut into 0.5-cm-thick coronal sections and stained with triphenyltetrazolium chloride to define areas of infarction. Treatment with either tissue plasminogen activator or urokinase significantly reduced the number of emboli present in the cerebral circulation (p less than 0.05). The area of ischemic injury was also significantly reduced (p less than 0.05) by acute fibrinolytic therapy with either tissue plasminogen activator or urokinase. However, only treatment with tissue plasminogen activator significantly reduced (p less than 0.05) the incidence of infarction. There was no evidence of intracerebral hemorrhage in any rabbit. Early fibrinolytic therapy improved outcome in this model of acute embolic stroke.
Stroke 1990 Nov
PMID:Effect of intra-arterial tissue plasminogen activator and urokinase on autologous arterial emboli in the cerebral circulation of rabbits [corrected]. 212 53

Embolic stroke was induced in rabbits using autologous blood clot. One hour after stroke, animals received heparin anticoagulation (AC) for five hours (acute AC) or five days (chronic AC). Animals received excessive AC (partial thromboplastin time greater than 3.0 times control), adequate AC (partial thromboplastin time, 1.2 to 2.5 times control), or saline. After the animals were killed, the brains were examined for macroscopic evidence of intracerebral hemorrhage. There was no significant increase over control in the incidence or severity of hemorrhage in any of the four treatment groups. The data suggest that heparin AC does not promote intracerebral hemorrhage after experimental embolic stroke.
 ...
PMID:Intracerebral hemorrhage after experimental embolic infarction. Anticoagulation. 363 95

Embolic stroke complicating systemic lupus erythematosus has been infrequently reported. We examined a 25-year-old woman who suddenly became hemiplegic. Two-dimensional echocardiography identified a source of emboli. At cardiac surgery, friable thrombotic vegetations were found adhering to the mitral valve leaflets, left ventricular septal wall, and chordae tendineae. At autopsy several weeks later, careful pathologic examination of the heart failed to reveal evidence of thrombus formation or endocarditis. An embolus identical in appearance to the thrombotic vegetations described at cardiac surgery was found lodged in the left middle cerebral artery underlying the recent brain infarction. To our knowledge, this is the first report of embolic stroke in systemic lupus erythematosus caused by extensive cardiac thrombus formation in the absence of underlying endocarditis.
 ...
PMID:Embolic stroke complicating systemic lupus erythematosus. 402 19

63 patients with mitral annulus calcification (MAC) were followed for an average of 3.4 years. Two patients experienced TIA, both ipsilateral to a previous endarterectomy site, and IV-DSA demonstrated normal extracranial vessels. There were 3 strokes (5%), all fatal, but none could be attributed to embolism. Embolic stroke due to MAC is rare and difficult to prove due to coexistent atherosclerosis. Associated cardiac conditions such as atrial fibrillation, which might increase the risk of embolism, usually occur with MAC greater than or equal to 5 mm. In many patients, MAC may be better viewed as a marker of generalized calcific atherosclerosis rather than as an immediate embolic source.
Stroke
PMID:Risk of stroke in patients with mitral annulus calcification. 647 29

Recent randomized studies have demonstrated that percutaneous transvenous mitral commissurotomy (PTMC) has similar efficacy compared to surgical commissurotomy. Compared with surgery, PTMC is associated with shorter hospital stays, reduced patient discomfort, and significantly lower costs. The challenge of PTMC remains to provide increased safety. The most serious risks of balloon commissurotomy include cardiac perforation and embolic stroke. The creation of severe mitral regurgitation also limits the effectiveness of the procedure and occasionally leads to the requirement for emergency mitral valve replacement. Since 1986, procedure-related mortality has ranged from 0-2.7% with lower mortality rates reported recently. The most frequent cause of procedure-related death has been left ventricular (LV) perforation. This is almost exclusively a complication associated with the double balloon technique, which requires LV guidewires. Cardiac perforation due to inadvertent atrial perforation during transseptal catheterization may occur with the Inoue technique as well, but this tends to be less severe and has not resulted in death. Embolic stroke has occurred in 1.1-5.4% of cases. The incidence of embolic events has been favorably influenced by routine preprocedure transesophageal echocardiography (TEE), eliminating patients with left atrial thrombi. Significant mitral regurgitation occurs in 3.3-10.5% of patients undergoing balloon mitral commissurotomy. Fortunately, mitral regurgitation infrequently requires emergency surgery (0.3-3.3% of cases). Iatrogenic atrial septal defects are usually of no clinical consequence. Their frequency has been reduced with the use of the Inoue balloon catheter system and they rarely require surgical repair.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Complications related to percutaneous transvenous mitral commissurotomy. 799 42

The pathophysiology of stroke in humans is much more complex than what is typically studied in animal models. Embolic stroke models are more complex than pure ischemia models, but are more representative of human disease and may be particularly useful in the study of new therapeutic strategies. Vascular damage is a prominent feature of embolic stroke, and may be a useful therapeutic target. Serotonin antagonists, adenosine-regulating agents, free radical scavengers, matrix metalloproteinase inhibitors, and HMG-CoA reductase inhibitors are all potentially valuable agents in treating vascular damage after stroke. These agents facilitate decreased infarction volume, hemorrhage, and improved cerebral bloodflow.
 ...
PMID:Endothelium-targeted pharmacotherapeutics for the treatment of stroke. 1213 9

Embolic stroke is thought to cause irreparable damage in the brain immediately adjacent to the region of reduced blood perfusion. Therefore, much of the current research focuses on treatments such as anti-inflammatory, neuroprotective, and cell replacement strategies to minimize behavioral and physiological consequences. In the present study, intravenous delivery of human umbilical cord blood cells (HUCBC) 48 h after a middle cerebral artery occlusion (MCAo) in a rat resulted in both behavioral and physiological recovery. Nissl and TUNEL staining demonstrated that many of the neurons in the core were rescued, indicating that while both necrotic and apoptotic cell death occur in ischemia, it is clear that apoptosis plays a larger role than first anticipated. Further, immunohistochemical and histochemical analysis showed a diminished and/or lack of granulocyte and monocyte infiltration and astrocytic and microglial activation in the parenchyma in animals treated with HUCBC 48 h poststroke. Successful treatment at this time point should offer encouragement to clinicians that a therapy with a broader window of efficacy may soon be available to treat stroke.
 ...
PMID:Timing of cord blood treatment after experimental stroke determines therapeutic efficacy. 1671 56

Astrocytes support neurons not only physically but also chemically by secreting neurotrophic factors and energy substrates. Moreover, astrocytes establish a glial network and communicate through gap junctions in the brain. Connexin 43 (Cx43) is one of major component proteins in astrocytic gap junctions. Heterozygote Cx43 KO mice and astrocyte specific Cx43 KO mice exhibited amplified brain damage after ischemic insults, suggesting a neuroprotective role for astrocytic gap junctions. However, some reports mentioned unfavorable effects of gap junctions in neuronal support. Therefore, the role of astrocytic gap junctions under ischemic condition remains controversial. Since these studies have been performed using animal models, we investigated the Cx43 expression in human brain after stroke. Brain slice sections were prepared from pathological samples in our hospital. Embolic stroke brains sectioned because of the stroke were considered as acute ischemic models. Multiple infarction brains sectioned because of pneumonia or cancer were considered as chronic models. We observed the levels of Cx43 in both lesioned and intact areas, and compared them with acute and chronic models. As the results, astrocytes were strongly activated in penumbral lesions both of acute and chronic ischemic models. The Cx43 immunoreactivity was significantly amplified in the penumbra of chronic model compared to that of the acute model. Neurons were well preserved in chronic model compared to acute model. These findings suggested that the brain may generate neuronal protection by increasing the levels of Cx43 and amplifying the astrocytic gap junctional intercellular communication under hypoxic condition.
 ...
PMID:Enhanced connexin 43 immunoreactivity in penumbral areas in the human brain following ischemia. 1688

Uncoupling proteins (UCPs) are reported to regulate mitochondrial respiration and energy metabolism during hibernation. Recently, it has been reported that UCP2 and UCP5 might reduce free radical stress in the ischemic condition in in vitro models, suggesting both as potential neuroprotective agents. We therefore investigated the levels of UCP2 and UCP5 expression in the lesion of human brain infarction. Brain slice sections were prepared from pathological samples collected at our hospital. Embolic stroke brains sectioned because of the stroke (n = 5) and multiple brain infarction with several stroke episodes (n = 4) were selected for this study. We observed the amount of UCP2 and UCP5 expression in both lesioned and intact areas, and compared them between embolic stroke and multiple infarction cases. The results showed that the expression of UCP2 and UCP5 was significantly elevated in the ischemic lesions compared to the intact area. UCP5 expression in the lesions was higher in multiple infarction cases than in embolic stroke cases. In conclusion, brains may respond to neuroprotection through the increased expression of UCP2 and UCP5 under ischemic conditions. Moreover, UCP5 may respond to repetitive ischemic stresses or have a long-term effect.
 ...
PMID:Amplified expression of uncoupling proteins in human brain ischemic lesions. 1801 77

A 26-year-old man admitted with dysphasia and bilateral headache for three days. He had no known risk factors for stroke. Transthoracic two-dimensional echocardiography showed prominent trabeculations, with deep intertrabecular recesses in apex of the right ventricle. The multi-detector-row spiral cerebral computerized tomography revealed a little infarction in bilateral temporal and frontal lobe. The main mechanisms of neurovascular complications in NVM may be related to development of thrombi in the intertrabecular space. Extensively trabeculated ventricle, depressed systolic function, and/or the development of atrial fibrillation are the causes for thrombus formation7. Embolic stroke has been only rarely described in association with NVM9. However, whether NVM is a risk factor for stroke is controversially discussed. Prevention of embolic complications is an important management issue, and several authors have recommended long-term prophylactic anticoagulation for patients in NVM with atrial fibrillation and severe systolic dysfunction. The field of neurovascular complications, and specially cerebral infarction, in NVM of right ventricular remains not yet fully understood.
 ...
PMID:Cerebral infarction and right ventricular noncompaction. 1932 Dec 11


1 2 3 4 Next >>