The Rheology of the Carotid Sinus: A Path Toward Bioinspired Intervention

Iskander, Andrew; Bilgi, Coşkun; Naftalovich, Rotem; Hacihaliloglu, Ilker; Berkman, Tolga; Naftalovich, Daniel; Pahlevan, Niema M.

doi:10.3389/fbioe.2021.678048

Cited by 7 publications

(5 citation statements)

References 125 publications

(160 reference statements)

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“…The SVRR is the physiologic antagonist of the renin-angiotensin-aldosterone system (RAAS). Input into the RAAS comes from the carotid sinus, which senses wall shear stress [ 7 ]. The dilatation of the carotid sinus causes a preferential flow pattern that amplifies wall shear stress, making it sensitive to changes in small changes in wall shear stress.…”

Section: Discussionmentioning

confidence: 99%

New Onset Anemia, Worsened Plasma Creatinine Concentration, and Hyperviscosity in a Patient With a Monoclonal IgM Paraprotein

Sloop¹,

Moore²,

Pop³

et al. 2023

Cureus

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A 76-year-old female followed closely for five years with IgM monoclonal gammopathy of uncertain significance developed anemia, worsened plasma creatinine concentration, and markedly elevated serum viscosity. This case illustrates the scope of pathology that can be caused by elevated blood viscosity. Our patient’s anemia was a homeostatic response to normalize systemic vascular resistance and resulted from activation of the systemic vascular resistance response. The elevated plasma creatinine resulted from decreased renal perfusion because of elevated blood viscosity. Recent insights in hemorheology (the study of blood flow) are discussed, namely the recent identification of preferential blood flow patterns and erythrocyte autoregulation of deformability. These insights confirm that blood viscosity is part of the “milieu intérieur.”

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Section: Discussionmentioning

confidence: 99%

New Onset Anemia, Worsened Plasma Creatinine Concentration, and Hyperviscosity in a Patient With a Monoclonal IgM Paraprotein

Sloop¹,

Moore²,

Pop³

et al. 2023

Cureus

View full text Add to dashboard Cite

show abstract

“…We also utilized Newtonian flow assumption for the fluid in this study. This assumption is still conventionally used in both experimental and CFD studies in large arteries ( Iskander et al, 2021 ). However, future studies are needed to investigate the significance of non-Newtonian flow behavior in TBAD modeling in terms of FL flow reversal after TEVAR.…”

Section: Discussionmentioning

confidence: 99%

Model-Based Fluid-Structure Interaction Approach for Evaluation of Thoracic Endovascular Aortic Repair Endograft Length in Type B Aortic Dissection

Aghilinejad

Wei

Magee

et al. 2022

Front. Bioeng. Biotechnol.

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Thoracic endovascular aortic repair (TEVAR) is a commonly performed operation for patients with type B aortic dissection (TBAD). The goal of TEVAR is to cover the proximal entry tear between the true lumen (TL) and the false lumen (FL) with an endograft to induce FL thrombosis, allow for aortic healing, and decrease the risk of aortic aneurysm and rupture. While TEVAR has shown promising outcomes, it can also result in devastating complications including stroke, spinal cord ischemia resulting in paralysis, as well as long-term heart failure, so treatment remains controversial. Similarly, the biomechanical impact of aortic endograft implantation and the hemodynamic impact of endograft design parameters such as length are not well-understood. In this study, a fluid-structure interaction (FSI) computational fluid dynamics (CFD) approach was used based on the immersed boundary and Lattice–Boltzmann method to investigate the association between the endograft length and hemodynamic variables inside the TL and FL. The physiological accuracy of the model was evaluated by comparing simulation results with the true pressure waveform measurements taken during a live TEVAR operation for TBAD. The results demonstrate a non-linear trend towards increased FL flow reversal as the endograft length increases but also increased left ventricular pulsatile workload. These findings suggest a medium-length endograft may be optimal by achieving FL flow reversal and thus FL thrombosis, while minimizing the extra load on the left ventricle. These results also verify that a reduction in heart rate with medical therapy contributes favorably to FL flow reversal.

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“…Wall shear stress is detected by endothelial mechanoreceptors. Neural output from the carotid sinus is transmitted to the brainstem via the glossopharyngeal nerve (cranial nerve IX) [16], where it influences sympathetic output to the kidney.…”

Section: Control Of Blood Viscositymentioning

confidence: 99%

Hormonal Control of Blood Viscosity

Sloop,

Pop,

Weidman

et al. 2024

Cureus

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The hemodynamic milieu differs throughout the vascular tree because of varying vascular geometry and blood velocities. Accordingly, the risk of turbulence, which is dictated by the Reynolds and Dean numbers, also varies. Relatively high blood viscosity is needed to prevent turbulence in the left ventricle and aorta, where high-velocity blood changes direction several times. Low blood viscosity is needed in the capillaries, where erythrocytes pass through vessels with a diameter smaller than their own. In addition, higher blood viscosity is necessary when the cardiac output and peak blood velocity increase as a part of a sympathetic response or anemia, which occurs following significant hemorrhage. Blood viscosity, as reflected in systemic vascular resistance and vascular wall shear stress, is sensed, respectively, by cardiomyocyte stretching in the left ventricle and mechanoreceptors for wall shear stress in the carotid sinus. By controlling blood volume and red blood cell mass, the renin-aldosterone-angiotensin system and the systemic vascular resistance response control the hematocrit, the strongest intrinsic determinant of blood viscosity. These responses provide gross control of blood viscosity. Fine-tuning of blood viscosity in transient conditions is provided by hormonal control of erythrocyte deformability. The short half-life of some of these hormones limits their activity to specific vascular beds. Hormones that modulate blood viscosity include erythropoietin, angiotensin II, brain natriuretic factor, epinephrine, prostacyclin E2, antidiuretic hormone, and nitric oxide.

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The Rheology of the Carotid Sinus: A Path Toward Bioinspired Intervention

Cited by 7 publications

References 125 publications

New Onset Anemia, Worsened Plasma Creatinine Concentration, and Hyperviscosity in a Patient With a Monoclonal IgM Paraprotein

New Onset Anemia, Worsened Plasma Creatinine Concentration, and Hyperviscosity in a Patient With a Monoclonal IgM Paraprotein

Model-Based Fluid-Structure Interaction Approach for Evaluation of Thoracic Endovascular Aortic Repair Endograft Length in Type B Aortic Dissection

Hormonal Control of Blood Viscosity

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