ABSTRACT
Embolic strokes make up a significant proportion of acute cerebrovascular accidents. Doppler blood flow monitoring with microembolodetection allows suggesting the embolic nature of cerebral infarction. The aim of this study was to identify factors associated with the presence of microembolic signals in patients with ischemic stroke. The study included 515 patients, microembolic signals were detected in 48 (9.3%) of them. According to multispiral CT angiography, significant differences in patients with and without microembolic signals were found for wall thickness of both common carotid arteries and for left internal carotid artery (p<0.05). Factor analysis revealed a variable that reflects the severity of left carotid arteries atherosclerosis, which was a significant predictor of registration of the microembolic signals (p=0.016).
Subject(s)
Carotid Stenosis , Intracranial Embolism , Ischemic Stroke , Stroke , Brain , Carotid Artery, Internal/diagnostic imaging , Carotid Stenosis/complications , Humans , Intracranial Embolism/complications , Intracranial Embolism/diagnostic imaging , Stroke/diagnostic imagingABSTRACT
We analyzed interrelations between the cerebral blood flow, cardiac output, and condition of the brain substance in 530 patients with ischemic stroke. Dependencies between the linear blood flow velocities in all arteries supplying the brain, as well as between the total volume blood flow through the internal carotid arteries and left ventricular stroke volume were revealed. The severity of atrophy was maximum in the parietal lobes (median 1.5 (1.0; 2.0)) and minimum in the occipital lobes (median 0.5 (0; 1.0)). Temporal lobes cortical atrophy significantly correlated with changes in the limbic system and in the periventricular and deep white matter; a significant weak inverse correlation of this parameter with blood flow in the middle cerebral artery was also found. Changes in the periventricular white matter (but not in deep white matter) demonstrated a significant inverse correlation with blood flow in the middle and anterior cerebral arteries.
Subject(s)
Cerebrovascular Circulation , Ischemic Stroke/physiopathology , Occipital Lobe/physiopathology , Temporal Lobe/physiopathology , White Matter/physiopathology , Adult , Aged , Aged, 80 and over , Anterior Cerebral Artery/diagnostic imaging , Anterior Cerebral Artery/physiopathology , Basilar Artery/diagnostic imaging , Basilar Artery/physiopathology , Blood Flow Velocity , Carotid Artery, Internal/diagnostic imaging , Carotid Artery, Internal/physiopathology , Female , Humans , Ischemic Stroke/diagnostic imaging , Limbic System/diagnostic imaging , Limbic System/physiopathology , Magnetic Resonance Angiography , Male , Middle Aged , Middle Cerebral Artery/diagnostic imaging , Middle Cerebral Artery/physiopathology , Neuroimaging , Occipital Lobe/diagnostic imaging , Posterior Cerebral Artery/diagnostic imaging , Posterior Cerebral Artery/physiopathology , Prospective Studies , Stroke Volume , Temporal Lobe/diagnostic imaging , Vertebral Artery/diagnostic imaging , Vertebral Artery/physiopathology , White Matter/diagnostic imagingABSTRACT
We analyzed the relationship between white matter hyperintensities in T2-weighted MR-images (according to Fazekas score) and the state of cognitive functions (total MOCA score) in 65 asymptomatic individuals. A relationship between the presence/number of lesions in the deep white matter of the brain and cognitive status according to the total MOCA score was revealed. The results of cognitive functions assessment also correlated with MRI evaluation of the severity of brain cortex atrophy. The severity of deep white matter lesions according to the Fazekas scale were also associated with end-diastolic blood flow velocities in the middle cerebral, vertebral, and basilar arteries.
Subject(s)
Brain/pathology , Cognition/physiology , Cognitive Dysfunction/physiopathology , White Matter/pathology , Adult , Brain/metabolism , Female , Humans , Magnetic Resonance Imaging , Male , Middle Aged , White Matter/metabolismABSTRACT
Human placenta mesenchymal stromal cells were injected to healthy rats either stereotaxically into the striatum or intra-arterially through the internal carotid artery. Some cells injected into the brain migrated along the corpus callosum both medially and laterally or concentrated around small blood vessels. A small fraction of MSC injected intra-arterially adhered to the endothelium and stayed inside blood vessels for up to 48 hours mostly in the basin of the middle cerebral artery. Neither stereotaxic, nor intra-arterial transplantation of mesenchymal stromal cells modulated the proliferation of neural stem cells in the subventricular zone of the brain, but stereotaxic transplantation suppressed activation of their proliferation in response to traumatization with the needle.
Subject(s)
Corpus Striatum/cytology , Lateral Ventricles/cytology , Mesenchymal Stem Cell Transplantation/methods , Mesenchymal Stem Cells/cytology , Neural Stem Cells/cytology , Placenta/cytology , Animals , Carotid Artery, Internal/cytology , Cell Movement , Cell Proliferation , Corpus Striatum/surgery , Female , Humans , Injections, Intra-Arterial , Injections, Intraventricular , Lateral Ventricles/surgery , Male , Mesenchymal Stem Cells/physiology , Middle Cerebral Artery/cytology , Neural Stem Cells/physiology , Placenta/physiology , Pregnancy , Primary Cell Culture , Rats , Rats, Wistar , Stereotaxic Techniques , Transplantation, HeterologousABSTRACT
Expression of inducible NO-synthase mRNA and myocardial infiltration with neutrophils were studied in rats with modeled permanent ischemia and ischemia/reperfusion models. Expression of inducible NO synthase mRNA in the ischemic region increased significantly in 3, 3.5, and 4 h in modeled ischemia/reperfusion and in 3.5 and 4 h in permanent ischemia. Myocardial infiltration with neutrophils was significantly higher than in intact controls throughout the experiment without significant intergroup differences. In non-ischemic myocardium, enhanced expression of inducible NO synthase mRNA and moderate neutrophilic-lymphocytic myocardial infiltration were also observed in 3.5, and 4 h after ischemia.
Subject(s)
Lymphocytes/immunology , Myocardial Reperfusion Injury/genetics , Myocardium/enzymology , Neutrophils/immunology , Nitric Oxide Synthase Type II/genetics , RNA, Messenger/genetics , Animals , Animals, Outbred Strains , Cell Movement , Gene Expression Regulation , Lymphocytes/cytology , Male , Myocardial Reperfusion Injury/enzymology , Myocardial Reperfusion Injury/immunology , Myocardial Reperfusion Injury/pathology , Myocardium/immunology , Myocardium/pathology , Neutrophil Infiltration , Neutrophils/cytology , Nitric Oxide Synthase Type II/metabolism , RNA, Messenger/metabolism , Rats , Time FactorsABSTRACT
The effect of peptide Semax on remodeling of cardiac sympathetic innervation was examined in rats with experimental myocardial infarction. In 28 days after ischemia/reperfusion injury, Semax diminished the growth of sympathetic innervation of ventricular septum, although it produced no effect on the density of ß1 and ß2 adrenoceptors.
Subject(s)
Myocardial Infarction/metabolism , Prostatitis/metabolism , Adrenocorticotropic Hormone/analogs & derivatives , Adrenocorticotropic Hormone/therapeutic use , Animals , Male , Myocardial Infarction/drug therapy , Peptide Fragments/therapeutic use , Prostate/drug effects , Prostate/metabolism , Prostate/pathology , Prostatitis/drug therapy , Quercetin/analogs & derivatives , Quercetin/therapeutic use , Rats , Rats, Wistar , Sympathetic Nervous System/drug effects , Sympathetic Nervous System/metabolism , Sympathetic Nervous System/pathologyABSTRACT
Activation of the sympathetic nervous system aggravates the course of myocardial infarction. Semax peptide moderated the degree of this activation and prevented the increase in the density of sympathetic endings in rat caudal artery in 28 days after ischemia or ischemia/reperfusion. The peptide reduced the density of α-adrenoreceptors in the caudal artery of rats with myocardial infarction. Semax produced no effect on ß-adrenoreceptors in both experimental models. The experiments on isolated segments of the caudal artery revealed reduced vascular responsiveness to electrical stimulation and norepinephrine infusion in rats treated with Semax after ischemia/reperfusion injury.
Subject(s)
Adrenocorticotropic Hormone/analogs & derivatives , Myocardial Infarction/drug therapy , Myocardial Infarction/metabolism , Peptide Fragments/pharmacology , Peptide Fragments/therapeutic use , Sympathetic Nervous System/drug effects , Sympathetic Nervous System/metabolism , Adrenocorticotropic Hormone/pharmacology , Adrenocorticotropic Hormone/therapeutic use , Animals , Electric Stimulation , Male , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Norepinephrine/pharmacology , Norepinephrine/therapeutic use , Rats , Receptors, Adrenergic, beta/metabolismABSTRACT
Monocyte chemotactic protein-1 (MCP-1) is a chemokine that stimulates monocytes and macrophage migration into the sites of acute of chronic inflammation. Our study shows morphological changes in ischemic myocardium followed by the administration of two synthetic structural fragments of MCP-1 that are monocyte/macrophage migration inductor peptide IX and peptide X an inhibitor. Results show that peptides can change time points of the inflammatory response in myocardium. Peptide IX administration leads to increased and accelerated inflammatory response, i. e. attracts an additional number of monocytes and macrophages into the inflammatory focus. The introduction of the peptide X observed prolonged inflammatory process with the overall gain signs of myocardial damage.
