Cardioprotective Effect of p-Tyrosol in the Acute Period of Cardiovascular and Cerebral Ischemia

2019 ◽  
Keyword(s):  
Cerebral Ischemia ◽  
Cardioprotective Effect ◽  
Acute Period

scholarly journals On the Question of the Reflexotherapy Action Mechanisms in the Ischemic Stroke Acute Period (Literature Review)

2021 ◽  
Vol 20 (6) ◽  
pp. 67-75
Author(s):  
Elena E. Molchanova ◽  
Victoria V. Polunina ◽  
Boris A. Polyaev ◽  
Valery P. Plotnikov ◽  
Andrey N. Lobov ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Economic Losses ◽  
Stroke Patients ◽  
Cerebrovascular Reserve ◽  
Acute Period ◽  
Mediators Of Inflammation ◽  
Acute Cerebral Ischemia ◽  
Degree Of Disability ◽  
Underlying Mechanisms

A high degree of disability in stroke patients, along with severe social and economic losses, determine the enduring urgency of the problem of early rehabilitation for post-stroke patients. Despite the proven effectiveness of the various reflexotherapy techniques in rehabilitation of patients with ischemic stroke, the underlying mechanisms remain unclear. The aim of the review was to analyze the mechanisms of the acupuncture intervention effect on the main links of the ischemic stroke pathogenesis, on neurological deficit and the volume of cerebral infarction (based on publications in international databases). The use of acupuncture in the acute period of ischemic stroke can improve the ability to cerebrovascular reserve, reduce the severity of arterial stiffness and endothelial dysfunction, induce neuroprotection, inhibit cell apoptosis and stimulate neuroplasticity, alleviate the inflammatory response in acute cerebral ischemia, regulate mediators of inflammation and oxidative stress etc., thus improving cerebral blood flow. The analysis of literature data has shown that acupuncture induces multilevel regulation through complex mechanisms, and one factor may not be enough to explain the positive effect against cerebral ischemia.

scholarly journals Acute impairment of saccadic eye movements is associated with delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

2017 ◽  
Vol 127 (4) ◽  
pp. 754-760
Author(s):  
Matthew J. Rowland ◽  
Payashi Garry ◽  
Jon Westbrook ◽  
Rufus Corkill ◽  
Chrystalina A. Antoniades ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Eye Movements ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Saccadic Eye Movements ◽  
T Test ◽  
Saccadic Latency ◽  
Acute Period

OBJECTIVEDelayed cerebral ischemia (DCI) causing cerebral infarction remains a significant cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (aSAH). Early brain injury in the first 72 hours following rupture is likely to play a key role in the pathophysiology underlying DCI but remains difficult to quantify objectively. Current diagnostic modalities are based on the concept of vasoconstriction causing cerebral ischemia and infarction and are either invasive or have a steep learning curve and user variability. The authors sought to determine whether saccadic eye movements are impaired following aSAH and whether this measurement in the acute period is associated with the likelihood of developing DCI.METHODSAs part of a prospective, observational cohort study, 24 male and female patients (mean age 53 years old, range 31–70 years old) were recruited. Inclusion criteria included presentation with World Federation of Neurosurgical Societies (WFNS) Grades 1 or 2 (“good grade”) aSAH on admission and endovascular treatment within 72 hours of aneurysmal rupture. DCI and DCI-related cerebral infarction were defined according to consensus guidelines. Saccadometry data were collected at 3 time points in patients: in the first 72 hours, between Days 5 and 10, and at 3 months after aSAH. Data from 10 healthy controls was collected on 1 occasion for comparison.RESULTSAge-adjusted saccadic latency in patients was significantly prolonged in the first 72 hours following aSAH when compared with controls (188.7 msec [95% CI 176.9–202.2 msec] vs 160.7 msec [95% CI 145.6–179.4 msec], respectively; p = 0.0054, t-test). By 3 months after aSAH, there was no significant difference in median saccadic latency compared with controls (188.7 msec [95% CI 176.9–202.2 msec] vs 180.0 msec [95% CI 165.1–197.8 msec], respectively; p = 0.4175, t-test). Patients diagnosed with cerebral infarction due to DCI had a significantly higher age-adjusted saccadic latency in the first 72 hours than those without infarction (240.6 msec [95% CI 216.7–270.3 msec] vs 204.1 msec [95% CI 190.7–219.5 msec], respectively; p = 0.0157, t-test). This difference was more pronounced during Days 5–10 following aSAH, the peak incidence for DCI (303.7 msec [95% CI 266.7–352.7 msec] vs 207.6 msec [95% CI 193.7–223.6 msec], respectively; p < 0.0001, t-test). A binary generalized linear model showed that latency in the first 72 hours was the only significant predictor of cerebral infarction (p = 0.0185).CONCLUSIONSThis is the first study to use saccadometry to measure the saccadic latency of eye movements in patients with aSAH during the acute period following aneurysm rupture. The results showed that median saccadic latency is associated with the risk of developing cerebral infarction due to DCI and may act as a potential objective biomarker to guide the need for intensive care admission and treatment. Future studies will look to formally validate saccadic latency as a biomarker of DCI in a larger cohort and assess whether the addition of saccades improves current clinical models for predicting patients at risk.

Ultrastorcture of Cerebellar Purkinje Cells in Rats Subjected To Partial Global Cerebral Ischemia

1985 ◽  
Vol 43 ◽  
pp. 674-675
Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros
Keyword(s):  
Cerebral Ischemia ◽  
Purkinje Cells ◽  
Cell Types ◽  
Microscopic Level ◽  
Global Cerebral Ischemia ◽  
Light Microscopic Level ◽  
Cerebellar Damage ◽  
Cerebellar Injury ◽  
Cerebellar Purkinje Cells ◽  
Cell Changes

In severe cerebral ischemia, Purkinje cells of the cerebellum are one of the cell types most vulnerable to anoxic damage. In the partial (forebrain) global ischemic (PGI) model of the rat, Paljärvi noted at the light microscopic level that cerebellar damage is inconsistant and when present, milder than in the telencephalon, diencephalon and rostral brain stem. Cerebellar injury was observed in 3 of 4 PGI rats following 5 minutes of reperfusion but in none of the rats after 90 min of reperfusion. To evaluate a time between these two extremes (5 and 90 min), the present investigation used the PGI model to study the effects of ischemia on the ultrastructure of cerebellar Purkinje cells in rats that were sacrificed after 30 min of reperfusion. This time also was chosen because lactic acid that is thought to contribute to ischemic cell changes in PGI is at a maximum after 30 min of reperfusion.

PPAR-γ agonist rosiglitazone decreases focal cerebral ischemia-induced inflammation and brain damage in adult mice

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S94-S94
Author(s):  
Kudret Tureyen ◽  
Ramya Sundaresan ◽  
Kellie Bowen ◽  
Raghu Vemuganti
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Adult Mice ◽  
Ppar Γ
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