Direct relationship between blood pressure and blood viscosity in normal and hypertensive subjects

Letcher, R. L.; Chien, Shu; Pickering, Thomas G.; Sealey, Jean E.; Laragh, John H.

doi:10.1016/0002-9343(81)90827-5

Cited by 318 publications

(173 citation statements)

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“…5,7,8,10,22 In most clinical patient populations, hypertension is associated with relative hyperviscosity, 5,7,8,10,22 but it is not clear if this is a cause or effect of high blood pressure, 9,23 or how previous treatment affects this relation. 9,11 In addition to being part of vascular resistance that thereby directly influences arterial pressure, higher WBV might also be a consequence of high blood pressure caused by increased filtration pressure, leading to hemoconcentration 24 -26 or to direct deterioration of rheological variables.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] Given the direct role of whole blood viscosity (WBV) in determining vascular resistance, recognized by Poiseuille, 4 there is interest in possible relations between viscosity and hypertension. [5][6][7][8][9][10][11] A study performed in normotensive subjects 6 demonstrated an independent association of WBV with diastolic or mean blood pressure, but not with systolic pressure, giving support to further research to investigate possible relations of WBV with hypertension and other cardiovascular risk factors. However, most mechanisms remain unclear.…”

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confidence: 99%

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Association of Blood Pressure With Blood Viscosity in American Indians

et al. 2005

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Abstract-Abnormalities in whole blood viscosity (WBV) have been implicated in hypertension. This study analyzes relations between WBV and blood pressure in the Strong Heart Study population of American Indians. We examined 676 participants (489 women, age 62Ϯ7 years) without prevalent cardiovascular disease or use of antihypertensive medications, digoxin, or aspirin. WBV was calculated from hematocrit and plasma protein concentration, at a shear rate of 208 seconds Ϫ1, by a validated equation. Forty eight percent of participants were obese, 43% had diabetes, 19% had hypertension, and 30% were current smokers. WBV was higher in men, smokers, and participants with central obesity, but it was not associated with hypertension or diabetes, even accounting for confounders. After adjusting for gender, age, center, smoking, obesity, diabetes, and plasma creatinine, WBV was negatively related to pulse pressure (␤ϭϪ0.13; PϽ0.001) and systolic pressure (␤ϭϪ0.09; PϽ0.02), mainly because of negative relations with hematocrit (␤ϭϪ0.11 and Ϫ0.10). Among hypertensive individuals, pulse pressure was positively related to age, diabetes, and female gender but not to WBV (multiple Rϭ0.63; PϽ0.0001); in contrast, in normotensive individuals, pulse pressure was related negatively to WBV or hematocrit, independent of body mass index, without relation to diabetes (Rϭ0.42; PϽ0.0001). Thus, under normal physiological conditions, in vivo WBV is negatively related pulse pressure. In contrast, the presence of arterial hypertension makes this relation less evident. Abnormalities in blood viscosity have been implicated in a number of cardiovascular diseases. 1-3 Given the direct role of whole blood viscosity (WBV) in determining vascular resistance, recognized by Poiseuille, 4 there is interest in possible relations between viscosity and hypertension. 5-11 A study performed in normotensive subjects 6 demonstrated an independent association of WBV with diastolic or mean blood pressure, but not with systolic pressure, giving support to further research to investigate possible relations of WBV with hypertension and other cardiovascular risk factors. However, most mechanisms remain unclear. 10 Unfortunately, direct determination of in vitro WBV is technically demanding and difficult to apply in epidemiological studies. We have previously shown that up to 83% of variability of WBV could be explained by microhematocrit and total plasma protein concentration (as a surrogate of plasma viscosity) over a range of shear rates from 0.1 to 208 seconds Ϫ1 . 6Relations between blood pressure and rheological components or WBV have rarely been studied in general populations. 12,13 The Strong Heart Study is a population-based longitudinal survey in American Indians, an ethnic group with higher prevalence of obesity and diabetes than in previous studies on WBV, which provides an opportunity to investigate cross-sectional associations between blood pressure and estimated WBV in the presence of these increasingly prevalent cardiovascular risk factors, without con...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Association of Blood Pressure With Blood Viscosity in American Indians

et al. 2005

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“…Hypertensive patients have higher Hct values than normotensive control individuals (23). Patients suffering from polycythemia vera or other erythrocytoses present with pathologically high Hcts leading to hypertension, thromboembolism, and other severe clinical complications (2,15).…”

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confidence: 99%

Paradoxical hypotension following increased hematocrit and blood viscosity

Martini¹,

Carpentier²,

Negrete³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

106

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-Hematocrit (Hct) of awake hamsters and CD-1 mice was acutely increased by isovolemic exchange transfusion of packed red blood cells (RBCs) to assess the relation between Hct and blood pressure. Increasing Hct 7-13% of baseline decreased mean arterial blood pressure (MAP) by 13 mmHg. Increasing Hct above 19% reversed this trend and caused MAP to rise above baseline. This relationship is described by a parabolic function (R 2 ϭ 0.57 and P Ͻ 0.05). Hamsters pretreated with the nitric oxide (NO) synthase (NOS) inhibitor N -nitro-L-arginine methyl ester (L-NAME) and endothelial NOS-deficient mice showed no change in MAP when Hct was increased by Ͻ19%. Nitrate/nitrite plasma levels of Hct-augmented hamsters increased relative to control and L-NAME treated animals. The blood pressure effect was stable 2 h after exchange transfusion. These findings suggest that increasing Hct increases blood viscosity, shear stress, and NO production, leading to vasodilation and mild hypotension. This was corroborated by measuring A1 arteriolar diameters (55.0 Ϯ 21.5 m) and blood flow in the hamster window chamber preparation, which showed statistically significant increased vessel diameter (1.04 Ϯ 0.1 relative to baseline) and microcirculatory blood flow (1.39 Ϯ 0.68 relative to baseline) after exchange transfusion with packed RBCs. Larger increases of Hct (Ͼ19% of baseline) led blood viscosity to increase Ͼ50%, overwhelming the NO effect through a significant viscosity-dependent increase in vascular resistance, causing MAP to rise above baseline values. nitric oxide; shear stress; vascular resistance; hypertension IT IS A GENERAL MEDICAL and clinical perception that an increase in blood viscosity may lead to short-and long-term negative physiological conditions, and there appears to be universal agreement that increased blood viscosity is a factor in hypertension. Lowering blood viscosity, however, is not advocated as a means for controlling hypertension with the exception of erythrocytosis, substantial Hct increases consequent to adaptation to high altitudes, and cardiovascular impairment in premature infants. These conditions represent extremes of an increase in blood viscosity and clearly must be corrected by lowering Hct, because the extreme excess of red blood cells (RBCs) is superfluous in providing adequate oxygen-carrying capacity and is in fact a hindrance to blood flow and therefore oxygen delivery.Clinical studies (14, 37) report a significant relationship between hypertension and high Hct levels. Hypertensive patients have higher Hct values than normotensive control individuals (23). Patients suffering from polycythemia vera or other erythrocytoses present with pathologically high Hcts leading to hypertension, thromboembolism, and other severe clinical complications (2, 15). There is evidence, however, that individuals, such as Peruvian miners, survive with Hct levels of 75-91% (18), suggesting the existence of an adaptive mechanism.Endothelial cells play a key role in the regulation of blood pressure and blood flow beca...

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“…3,4 Furthermore, epidemiological studies in populations containing both hypertensive and normotensive individuals have found an increased risk of cardiovascular disease in those with higher mean plasma viscosity levels. 5,6 Nevertheless, relatively little work has centred on the relationship between plasma viscosity, haematocrit and cardiovascular risk in hypertensive patients.…”

Section: Plasma Viscosity and Haematocritmentioning

confidence: 99%