Еffects of different doses of atorvastatin on platelet aggregation, endothelial function, levels of serotonin, angiotensin II, blood pressure, cerebral blood flow in hypertensive patients with hyperlipidemia

Cardiovascular diseases have been the leading causes of mortality in Taiwan and the world at large for decades. The composition of cardiovascular and cerebrovascular systems is quite complicated. Therefore, it is difficult to detect or trace the related signs of cardiovascular and cerebrovascular diseases. The characteristics and changes in cardiopulmonary system disease can be used to track cardiovascular and cerebrovascular disease prevention and diagnosis. This can effectively reduce the occurrence of cardiovascular and cerebrovascular diseases. This study analyzes the variability in blood pressure, cerebral blood flow velocity and the interaction characteristics using linear and nonlinear approaches in stroke, hypertension and healthy groups to identify the differences in cardiovascular control in these groups. The results showed that the blood pressure and cerebral blood flow of stroke patients and hypertensive patients were significantly higher than those of healthy people (statistical differences (p < 0.05). The cerebrovascular resistance (CVR) shows that the CVR of hypertensive patients is higher than that of healthy people and stroke patients (p < 0.1), indicating that the cerebral vascular resistance of hypertensive patients is slightly higher. From the patient’s blood flow and vascular characteristics, it can be observed that the cardiovascular system is different from those in healthy people. Baroreflex sensitivity (BRS) decreased in stroke patients (p < 0.05). Chaotic analysis revealed that the blood pressure disturbance in hypertensive patients has a higher chaotic behavior change and the difference in initial state sensitivity. Cross-correlation (CCF) analysis shows that as the course of healthy→hypertension→stroke progresses, the maximum CCF value decreases significantly (p < 0.05). That means that blood pressure and cerebral blood flow are gradually not well controlled by the self-regulation mechanism. In conclusion, cardiovascular control performance in hypertensive and stroke patients displays greater variation. This can be observed by the bio-signal analysis. This analysis could identify a measure for detecting and preventing the risk for hypertension and stroke in clinical practice. This is a pilot study to analyze cardiovascular control variation in healthy, hypertensive and stroke groups.

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Angiotensin II, hypertension and angiotensin II receptor antagonism: Roles in the behavioural and brain pathology of a mouse model of Alzheimer's disease

Journal of Cerebral Blood Flow & Metabolism ◽

10.1177/0271678x16667364 ◽

2016 ◽

Vol 37 (7) ◽

pp. 2396-2413 ◽

Cited By ~ 17

Author(s):

Maximilian Wiesmann ◽

Monica Roelofs ◽

Robert van der Lugt ◽

Arend Heerschap ◽

Amanda J Kiliaan ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Blood Pressure ◽

Alzheimer's Disease ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Angiotensin Ii ◽

Functional Connectivity ◽

Wild Type ◽

Angiotensin Ii Receptor ◽

Induced Hypertension

Elevated angiotensin II causes hypertension and contributes to Alzheimer’s disease by affecting cerebral blood flow. Angiotensin II receptor blockers may provide candidates to reduce (vascular) risk factors for Alzheimer’s disease. We studied effects of two months of angiotensin II-induced hypertension on systolic blood pressure, and treatment with the angiotensin II receptor blockers, eprosartan mesylate, after one month of induced hypertension in wild-type C57bl/6j and AβPPswe/PS1ΔE9 (AβPP/PS1/Alzheimer’s disease) mice. AβPP/PS1 showed higher systolic blood pressure than wild-type. Subsequent eprosartan mesylate treatment restored this elevated systolic blood pressure in all mice. Functional connectivity was decreased in angiotensin II-infused Alzheimer’s disease and wild-type mice, and only 12 months of Alzheimer’s disease mice showed impaired cerebral blood flow. Only angiotensin II-infused Alzheimer’s disease mice exhibited decreased spatial learning in the Morris water maze. Altogether, angiotensin II-induced hypertension not only exacerbated Alzheimer’s disease-like pathological changes such as impairment of cerebral blood flow, functional connectivity, and cognition only in Alzheimer’s disease model mice, but it also induced decreased functional connectivity in wild-type mice. However, we could not detect hypertension-induced overexpression of Aβ nor increased neuroinflammation. Our findings suggest a link between midlife hypertension, decreased cerebral hemodynamics and connectivity in an Alzheimer’s disease mouse model. Eprosartan mesylate treatment restored and beneficially affected cerebral blood flow and connectivity. This model could be used to investigate prevention/treatment strategies in early Alzheimer’s disease.

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Patterns of Cerebral Blood Flow and Systemic Hemodynamics During Arithmetic Processing

Journal of Psychophysiology ◽

10.1027/0269-8803.22.2.81 ◽

2008 ◽

Vol 22 (2) ◽

pp. 81-90 ◽

Cited By ~ 21

Author(s):

Natalie Werner ◽

Neval Kapan ◽

Gustavo A. Reyes del Paso

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Time Course ◽

Doppler Sonography ◽

Transcranial Doppler Sonography ◽

Systemic Hemodynamics ◽

Heart Period ◽

Blood Flow Velocities ◽

Flow Velocities

The present study explored modulations in cerebral blood flow and systemic hemodynamics during the execution of a mental calculation task in 41 healthy subjects. Time course and lateralization of blood flow velocities in the medial cerebral arteries of both hemispheres were assessed using functional transcranial Doppler sonography. Indices of systemic hemodynamics were obtained using continuous blood pressure recordings. Doppler sonography revealed a biphasic left dominant rise in cerebral blood flow velocities during task execution. Systemic blood pressure increased, whereas heart period, heart period variability, and baroreflex sensitivity declined. Blood pressure and heart period proved predictive of the magnitude of the cerebral blood flow response, particularly of its initial component. Various physiological mechanisms may be assumed to be involved in cardiovascular adjustment to cognitive demands. While specific contributions of the sympathetic and parasympathetic systems may account for the observed pattern of systemic hemodynamics, flow metabolism coupling, fast neurogenic vasodilation, and cerebral autoregulation may be involved in mediating cerebral blood flow modulations. Furthermore, during conditions of high cardiovascular reactivity, systemic hemodynamic changes exert a marked influence on cerebral blood perfusion.

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