Effects of different doses of rosuvastatin on blood lipids, endothelial function, and cerebral blood flow in patients with hyperlipidemia and cerebral ischemic stroke

2015 ◽  
Vol 241 (1) ◽  
pp. e206
Author(s):  
M. Bubnova ◽  
D. Aronov ◽  
E. Semenova
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Ischemic Stroke ◽  
Endothelial Function ◽  
Blood Lipids ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Different Doses

scholarly journals Effects of different doses of rosuvastatin on blood lipids and lipoproteins, endothelial function, and cerebral blood flow in patients with hyperlipidemia and cerebral ischemic stroke-complicated hypertension

2013 ◽  
Vol 4 (2) ◽  
pp. 72-80
Author(s):  
M. G Bubnova ◽  
E. G Semenova ◽  
D. M Aronov ◽  
T. T Batysheva
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Ischemic Stroke ◽  
Blood Lipids ◽  
Ldl Cholesterol ◽  
End Products ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Lipids And Lipoproteins ◽  
The Impact

Objective: to study the dose-dependent effect of rosuvastatin on blood lipids and lipoproteins (LP), endothelial functional activity, coagulation, and safety parameters in patients with hyperlipidemia (HLP) and hypertension after cerebral ischemic stroke (CIS). Subjects and method. The trial included 34 patients (mean age 59,4±7,4 years) with types IIa or IIb HLP and CIS-complicated hypertension. The patients were randomized to 2 groups: 1) rosuvastatin 10 mg and 2) rosuvastatin 20 mg. The trial lasted 12 weeks. The dose of rosuvastatin remained unchanged throughout the trial. The authors evaluated the impact of therapy on the blood concentration of lipids, LP, fibrinogen, end products of nitric oxide (NO) metabolism, and endothelin-1 (ET-1), cerebral blood flow by great cerebral artery Doppler ultrasound data, as well as the parameters reflecting the safety of the therapy. Results. After 12-week therapy with rosuvastatin 10 and 20 mg, there was a significant decrease in the level of cholesterol by 30 and 35%, low-density lipoprotein (LDL) cholesterol by 40 and 45%, and triglycerides by 18 and 26%, respectively. Increasing the dose of rosuvastatin was attended by a significant rise (by 18%) in the number of patients with target LDL cholesterol levels. Rosuvastatin therapy caused no changes in the high baseline level of fibrinogen. At the same time, at the rosuvastatin doses of 10 and 20 mg, the concentrations of end products of NO metabolism increased by 14,3 and 12,4%, respectively. The vasoprotective effect of rosuvastatin 20 mg showed itself just at therapy week 6. Significantly decreased ET-1 levels were found when rosuvastatin was given in a dose of 10 mg; this was directly related to the baseline concentration of ET-1. In the patients who had an ET-1 level of >0,51 fmol/ml, its drop was 22,5% (p

scholarly journals Intra-Arterial Tirofiban Infusion for Partial Recanalization with Stagnant Flow in Hyperacute Cerebral Ischemic Stroke

2011 ◽  
Vol 17 (4) ◽  
pp. 442-451 ◽  
Author(s):  
S.K. Baik ◽  
S.J. Oh ◽  
K-P. Park ◽  
J-H. Lee
Keyword(s):  
Blood Flow ◽  
Ischemic Stroke ◽  
Clinical Status ◽  
Cerebral Stroke ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Antegrade Flow ◽  
Stagnant Flow ◽  
Iv Tpa

Early reocclusion is a major concern associated with poor clinical outcomes in patients with an ischemic cerebral stroke. This occurs most frequently in patients with partial initial recanalization. This study focuses on partial recanalization with stagnant antegrade flow after intravenous (IV) tPA or spontaneously, treated with the administration of intra-arterial (IA) tirofiban. Three patients with initial M1 occlusion on diagnostic studies had an occluded segment that was recanalized with stagnant flow after IV tPA or spontaneously. In all cases, IA tirofiban was administrated. We evaluated the distal blood flow and the degree of vascular narrowing in the pre and post-procedure angiography and at follow-up in addition to the clinical status. In all patients, severe vascular narrowing with stagnation of blood flow was detected in the initial M1. After infusion of IA tirofiban, improvement of the distal blood flow was achieved rapidly within 40 minutes in all patients. The severe vascular narrowing resolved rapidly in two patients without residual stenosis. In one patient, moderate vascular narrowing was still present. The median baseline National Institutes of Health Stroke Scale (NIHSS) scores were 18 and the median post-procedural NIHSS scores were 2 at two weeks. No intracerebral hemorrhage occurred in any of the patients. Treatment with IA tirofiban was safe and effective in patients with partial initial recanalization. It can be suggested that detection of any partial recanalization is time for administration of glycoprotein IIb-IIIa receptor inhibitor in hyperacute ischemic stroke.

Irisin Ameliorates Hypoxia/Reoxygenation-Induced Inflammation and Apoptosis in PC12 Cells by Inhibiting TLR4/MYD88 Signaling Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 329-336
Author(s):  
Wang Jinli ◽  
Xu Fenfen ◽  
Zheng Yuan ◽  
Cheng Xu ◽  
Zhang Piaopiao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Major Complication ◽  
Lactic Dehydrogenase ◽  
Dependent Manner ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Myd88 Signaling ◽  
Hypoxia Reoxygenation

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.

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