The Role of Blood Viscosity in Infectious Diseases

Sloop, Gregory D.; Mast, Quirijn de; Pop, Gheorghe; Weidman, Joseph J; Cyr, John A. St.

doi:10.7759/cureus.7090

Cited by 33 publications

(48 citation statements)

References 35 publications

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“…Thus, the combined actions of both Piezo1 and TRPV4 may contribute to the endothelial vascular barrier dysfunction in hypertension. Shear stress also accompanies increased viscosity of blood which is a risk factor for deep vein thrombosis ( 23 , 62 , 63 ). It will be interesting to determine if targeting Piezo1 or TRPV4 channels can improve either of these clinical conditions.…”

Section: Discussionmentioning

confidence: 99%

Piezo1 acts upstream of TRPV4 to induce pathological changes in endothelial cells due to shear stress

Swain

Liddle

2021

Journal of Biological Chemistry

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The ion channels Piezo1 and TRPV4 have both, independently, been implicated in high venous pressure– and fluid shear stress–induced vascular hyperpermeability in endothelial cells. However, the mechanism by which Piezo1 and TRPV4 channels execute the same function is poorly understood. Here we demonstrate that Piezo1 regulates TRPV4 channel activation in endothelial cells and that Piezo1-mediated TRPV4 channel opening is a function of the strength and duration of fluid shear stress. We first confirmed that either fluid shear stress or the Piezo1 agonist, Yoda1, led to an elevation in intracellular calcium ([Ca 2+ ] i ) and that application of the Piezo1 antagonist, GsMTx4, completely blocked this change. We discovered that high and prolonged shear stress caused sustained [Ca 2+ ] i elevation that was blocked by inhibition of TRPV4 channel opening. Moreover, Piezo1 stimulated TRPV4 opening through activation of phospholipase A2. TRPV4-dependent sustained [Ca 2+ ] i elevation was responsible for fluid shear stress–mediated and Piezo1-mediated disruption of adherens junctions and actin remodeling. Blockade of TRPV4 channels with the selective TRPV4 blocker, HC067047, prevented the loss of endothelial cell integrity and actin disruption induced by Yoda1 or shear stress and prevented Piezo1-induced monocyte adhesion to endothelial cell monolayers. These findings demonstrate that Piezo1 activation by fluid shear stress initiates a calcium signal that causes TRPV4 opening, which in turn is responsible for the sustained phase calcium elevation that triggers pathological events in endothelial cells. Thus, deleterious effects of shear stress are initiated by Piezo1 but require TRPV4.

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Section: Discussionmentioning

confidence: 99%

Piezo1 acts upstream of TRPV4 to induce pathological changes in endothelial cells due to shear stress

Swain

Liddle

2021

Journal of Biological Chemistry

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“…Although vessel diameter has been primarily linked with blood flow rate, in pathological conditions, the contributions of perfusion pressure and viscosity becomes greatly enhanced. It has been reported from studies that the viscosity of blood is directly proportional to the hemoconcentration and inversely proportional to the flow rate (Sloop et al, 2020). This implies that factors which increase blood constituents and decrease plasma water will elevate the viscosity of blood which will decrease flow rate and alter tissue perfusion (Chang et al, 2017;Sloop et al, 2020).…”

Section: Plasma Flow Ratementioning

confidence: 99%

“…The viscosity of blood is directly proportional to the hemoconcentration and inversely proportional to the flow rate. This implies that factors which increase blood constituents and decrease plasma will elevate the blood viscosity which will decrease flow rate and alter tissue perfusion (Chang et al, 2017;Sloop et al, 2020). There are adequate evidences on diabetes that the elevated blood viscosity is a pathogenetic factor of diabetic microangiopathy, altering microcirculation and leading to insufficient tissue nutrition (Grigoleit et al, 1973;Cho et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Effect of Diabetes Mellitus and Hypertension on Osmotic Fragility and Hemorheological Factors in Male Wistar Rats

et al. 2021

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Diabetes mellitus is a common risk factor for erythrocyte osmotic stress. This study was aimed at exploring the effect of streptozotocin (STZ)-induced diabetes mellitus and salt-induced hypertension on osmotic fragility and hemorheological variables in male Wistar rats. Thirty male rats were grouped into five groups of six animals each as follows: negative control (zero salt in diet); positive control (normal salt diet - 0.3% salt); high salt diet (8% salt) (HSD only); STZ induced diabetes and normal salt diet (STZ only); STZ induced diabetes and high salt diet (STZ + HSD). At the end of a 4 weeks period, hematological variables, osmotic fragility, rheology and cardiovascular responses were assessed. There was an increase (p<0.05) in the mean arterial pressure and heart rate of HSD, STZ and HSD + STZ groups indicating a salt induced hypertension. There was a decrease in the body weight of STZ and HSD +STZ groups. There was significant increase (p<0.05) in the haematocrit, platelets estimates and fibrinogen concentrations in the experimental groups when compared with the controls. The STZ and STZ + HSD groups showed a reduced clotting time which corresponded to the increased platelet estimates and fibrinogen concentration. The increase in haematocrit, platelet and plasma protein resulted in the increased blood viscosity and a decreased flow rate. The osmotic fragility test was also observed to be increased (p<0.05) in HSD, STZ only and STZ + HSD groups. Diabetes mellitus and hypertension increase the rate of hemolysis of erythrocyte, as well as increase blood viscosity.

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“…Hemorheological disturbances, such as increased BV, are caused by decreased erythrocyte deformability, as occurs in malaria. Increased BV contributes to the association of acute infections with myocardial infarction (MI), venous thrombosis, and venous thromboembolism 23 . According to Sloop et al, 23 increased BV also increases vascular resistance, which decreases tissue perfusion and activates stretch receptors in the left ventricle, thereby initiating the systemic vascular resistance response, thus compensating for the increased vascular resistance by vasodilation, lowering hematocrit, and decreasing intravascular volume.…”

Section: Discussionmentioning

confidence: 99%

“…Increased BV contributes to the association of acute infections with myocardial infarction (MI), venous thrombosis, and venous thromboembolism 23 . According to Sloop et al, 23 increased BV also increases vascular resistance, which decreases tissue perfusion and activates stretch receptors in the left ventricle, thereby initiating the systemic vascular resistance response, thus compensating for the increased vascular resistance by vasodilation, lowering hematocrit, and decreasing intravascular volume. This physiological response causes the anemias associated with malaria, chronic inflammation, and other chronic diseases.…”

Section: Discussionmentioning

confidence: 99%

Standardization for obtaining blood viscosity: A systematic review

Arruda

Silva

Galduróz

et al. 2021

European J of Haematology

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Introduction There is evidence to suggest that blood viscosity (BV) is involved in several pathological processes. In this review, we evaluated the different methods of BV acquisition, analyzing the sample storage time, the storage temperature, the acquisition time, the acquisition temperature, sample volume, and shear rates, in order to standardize this technique. Methods We selected 50 articles with methods of obtaining BV, evaluating pathologies through BV, comparing rheological equipment, monitoring, and regulating BV. Results and conclusion Measurements should be obtained as soon as possible, to reduce hemorheological changes. It is necessary to refrigerate them at 4°C when the storage time is long. The acquisition time is related to the equipment used. BV measurements at 37°C will represent the real BV in vivo more faithfully. In order to understand the BV phenomena, the shear rates must be between 0.1 and 1000 s‐1. There is a wide variety of equipment available for measuring the BV.

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The Role of Blood Viscosity in Infectious Diseases

Cited by 33 publications

References 35 publications

Piezo1 acts upstream of TRPV4 to induce pathological changes in endothelial cells due to shear stress

Piezo1 acts upstream of TRPV4 to induce pathological changes in endothelial cells due to shear stress

Effect of Diabetes Mellitus and Hypertension on Osmotic Fragility and Hemorheological Factors in Male Wistar Rats

Standardization for obtaining blood viscosity: A systematic review

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