Hemorheological disturbances in cerebrovascular diseases

Velcheva, Irena; Antonova, Nadia; Titianova, Еkaterina; Damianov, Petar; Dimitrov, N.; Dimitrova, Valentina

doi:10.3233/ch-2008-1107

Cited by 26 publications

(12 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This study shows that rats with AlCl 3 -induced AD exhibited greater accumulation of Aβ-containing plaques in the hippocampus, cortex, and cerebral vessels, which increases vascular resistance [42] , alters hemorheological behavior, and contributes to endothelial dysfunction and vasculopathy [43] , [44] . In addition, Aβ-containing plaque accumulation induces RBC aggregation and causes changes in the shear stress of the vessel wall, thereby increasing WBV.…”

Section: Discussionmentioning

confidence: 76%

Hemodynamic and Neuropathological Analysis in Rats with Aluminum Trichloride-Induced Alzheimer's Disease

et al. 2013

View full text Add to dashboard Cite

Background and AimsHemodynamic normality is crucial to maintaining the integrity of cerebral vessels and, therefore, preserving the cognitive functions of Alzheimer's disease patients. This study investigates the implications of the hemodynamic changes and the neuropathological diversifications of AlCl3-induced AD.MethodsThe experimental animals were 8- to 12-wk-old male Wistar rats. The rats were randomly divided into 2 groups: a control group and a (+)control group. Food intake, water intake, and weight changes were recorded daily for 22 wk. Synchronously, the regional cerebral blood flow (rCBF) of the rats with AlCl3-induced AD were measured using magnetic resonance imaging (MRI). The hemorheological parameters were analyzed using a computerized auto-rotational rheometer. The brain tissue of the subjects was analyzed using immunohistological chemical (IHC) staining to determine the beta-amyloid (Aβ) levels.ResultsThe results of hemodynamic analysis revealed that the whole blood viscosity (WBV), fibrinogen, plasma viscosity and RBC aggregation index (RAI) in (+)control were significantly higher than that of control group, while erythrocyte electrophoresis (EI) of whole blood in (+)control were significantly lower than that of control group. The results of acetylcholinesterase-RBC (AChE-RBC)in the (+)control group was significantly higher than that of the control group. The results also show that the reduction of rCBF in rats with AlCl3-induced AD was approximately 50% to 60% that of normal rats. IHC stain results show that significantly more Aβ plaques accumulated in the hippocampus and cortex of the (+)control than in the control group.ConclusionThe results accentuate the importance of hemorheology and reinforce the specific association between hemodynamic and neuropathological changes in rats with AlCl3-induced AD. Hemorheological parameters, such as WBV and fibrinogen, and AChE-RBC were ultimately proven to be useful biomarkers of the severity and progression of AD patients. In addition, the parameters can be substituted for invasive inspection in therapeutic intervention.

show abstract

Section: Discussionmentioning

confidence: 76%

Hemodynamic and Neuropathological Analysis in Rats with Aluminum Trichloride-Induced Alzheimer's Disease

et al. 2013

View full text Add to dashboard Cite

show abstract

“…In these conditions, blood viscosity is in the range of 60 millipoise or greater at a shear rate of 94.5/s. However, chronic lesser elevations of viscosity do occur (roughly, 50-56 millipoise at 94.5/s, normal being 37-49 millipoise at the same shear rate) [Antonova and Velcheva, 1999;Velcheva et al 2008]. Rosenson and colleagues reported a normal value of 32.6 millipoise at a shear rate of 100/s [Rosenson et al1996].…”

Section: Introductionmentioning

confidence: 99%

“…In the study of Antonova and Velcheva, viscosities in the range referred to here as 'chronic hyperviscosity' were associated with chronic cerebral infarctions, transient ischemic attacks, and risk factors for stroke [Antonova and Velcheva, 1999]. In Velcheva and colleagues' work, chronic hyperviscosity was associated with transient ischemic attacks and unilateral cerebral infarctions [Velcheva et al 2008].…”

Section: Introductionmentioning

confidence: 99%

The role of chronic hyperviscosity in vascular disease

Sloop

Holsworth²,

Weidman

et al. 2014

Therapeutic Advances in Cardiovascular Disease

View full text Add to dashboard Cite

BackgroundThe pathogenesis of vascular disease is complex and as of yet not totally understood. Conventional wisdom suggests that atherosclerotic cardiovascular disease is caused by the accumulation of lipid molecules in the arterial luminal wall. Various therapeutic modalities have been proposed; however, current treatment with cholesterol-lowering drugs has not completely solved this problem. Risk factors aiding in the development of atherosclerotic disease have been long promoted, such as genetics, dyslipidemia, hypertension, smoking, lack of adequate exercise, metabolic syndrome, and obesity. However, 50% of myocardial infarctions occur in subjects without overt hyperlipidemia, and 20% of myocardial infarctions occur in the absence of any classic risk factors [Ridker and Libby, 2011].The reason why the pathogenesis of chronic vascular diseases, including atherosclerosis, hypertension, and the metabolic syndrome, is not fully understood by the mainstream is because the role of blood viscosity has been ignored. Most physicians are aware of acute hyperviscosity syndromes as can be seen in Waldenstrom's macroglobulinemia, polycythemia vera, and leukemia, which require immediate intervention. In these conditions, blood viscosity is in the range of 60 millipoise or greater at a shear rate of 94.5/s. However, chronic lesser elevations of viscosity do occur (roughly, 50-56 millipoise at 94.5/s, normal being 37-49 millipoise at the same shear rate) [Antonova and Velcheva, 1999;Velcheva et al. 2008]. Rosenson and colleagues reported a normal value of 32.6 millipoise at a shear rate of 100/s [Rosenson et al.1996].States of chronic, lower elevations of viscosity are clinically less obvious, and left unappreciated, can ultimately shorten one's lifespan by contributing to cardiovascular disease. In the study of Antonova and Velcheva, viscosities in the range referred to here as 'chronic hyperviscosity' were associated with chronic cerebral infarctions, transient ischemic attacks, and risk factors for stroke [Antonova and Velcheva, 1999]. In Velcheva and colleagues' work, chronic hyperviscosity was associated with transient ischemic attacks and unilateral cerebral infarctions [Velcheva et al. 2008].It should be noted that the reference ranges for blood viscosity are tentative, and work remains in standardizing the reporting and measuring of blood viscosity. Hopefully, a collaboration similar to the Reference Values for Arterial Stiffness'The role of chronic hyperviscosity in vascular disease Gregory Sloop, Ralph E. Holsworth Jr, Joseph J. Weidman and John A. St Cyr Abstract: The pathogenesis of several major cardiovascular diseases, including atherosclerosis, hypertension, and the metabolic syndrome, is not widely understood because the role of blood viscosity is overlooked. Low-density lipoprotein accelerates atherosclerosis by increasing blood viscosity in areas of low flow or shear, predisposing to thrombosis. Atherosclerotic plaques are organized mural thrombi, as proposed by Duguid in the midtwentieth century. High-de...

show abstract

“…Nejznámější jsou vazospasmy [5], noční systémové hypotenze, redukce oční pulzní amplitudy a fluktuace očního perfuzního tlaku [25,27,32], úzké retinální vény [10]. Větší prevalence obstrukční spánkové apnoe/hypopnoe byla zaznamenána u NTG [22], dále větší výskyt mozkových cévních poruch [33] a myokardiálních infarktů [3], diabetes mellitus s poruchou periferního prokrvení [13]. Nemocní s NTG měli abnormální krevní parametry (vysoká viskozita krve, erytrocytární agregabilita, nízká rezistence erytrocytů a nízká deformalibita erytrocytů) ve srovnání se zdravou populací.…”

Section: Systémové Poruchyunclassified

Normal Tension vs High Tension Glaucoma: An Overview

Lešták

Pitrová

Nutterova

et al. 2019

CSO

View full text Add to dashboard Cite

The study provides an up-to-date overview of pathogenesis, functional and structural changes in normal tension glaucoma (NTG) and its differences from high tension glaucomas (HTG). The authors point to less known facts which make both diagnostic groups different. First of all, there are electrophysiological findings that verify pathology in the complete visual pathway in HTG in contrast to NTG where the retinal ganglion cell response is relatively normal but the abnormalities are in the visual pathway. This corresponds to the findings of functional magnetic resonance imaging of the brain with a significant decrease in activity in HTG compared to NTG. We found a higher decrease in activity in HTG following application of the colour paradigm compared to NTG where we did not see a similar difference. We also investigated the central corneal thickness (CCT) in both diagnostic groups. We did not find a statistically significant difference. However, we found the effect of CCT on progression of the changes in visual fields in HTG. In relation to suspicion of abnormally low cerebrospinal pressure and a possible cerebrovascular fluid flow disturbance in NTG, we examined the optic nerve thickness (OND) and optic nerve sheath diameter (OSD) at a distance of 4, 8, 16 and 20mm from the posterior pole of the eye. In the comparison with the healthy population, we did not find any abnormalities except for the width of the optic chiasma that was markedly lower in NTG. In relation to a possible impairment of cerebral perfusion we determined the degrees of cerebral atrophy using magnetic resonance imaging by measuring the bicaudate ratio (BCR) and white matter lesions using the Fazekas scale. We did not find a difference between HTG and NTG in BCR. We found statistically significant changes in BCR which correlated with the changes in visual fields. The higher values of the pattern defect were associated with increased brain atrophy (BCR). We did not detect similar relations in the Fazekas scale. We found a significant difference in this parameter among NTG, HTG and a control group. We found the most advanced changes in the patients with HTG. Conclusion: In HTG, impairment of retinal ganglion cells and subsequently also their axons, including visual cortex occurs because of a high intraocular pressure. In NTG, the retinal ganglion cells are relatively normal like the visual cortex, but alteration occurs in their axons. The cause is not a high intraocular pressure but most probably ischemia.

show abstract

Hemorheological disturbances in cerebrovascular diseases

Cited by 26 publications

References 13 publications

Hemodynamic and Neuropathological Analysis in Rats with Aluminum Trichloride-Induced Alzheimer's Disease

Hemodynamic and Neuropathological Analysis in Rats with Aluminum Trichloride-Induced Alzheimer's Disease

The role of chronic hyperviscosity in vascular disease

Normal Tension vs High Tension Glaucoma: An Overview

Contact Info

Product

Resources

About