Why the study?
Studies evaluating the correlation between changes in blood viscosity and blood pressure in animals under conditions of arterial hypertension had not been conducted.
Does blood viscosity correlate with mean arterial pressure in normotensive and spontaneously hypertensive rats?
Does blood viscosity correlate with mean arterial pressure in normotensive and spontaneously hypertensive rats?
In spontaneously hypertensive rats, mean arterial pressure passively follows changes in blood viscosity, likely due to impaired endothelium-dependent vasodilation.
May inform viscosity-BP mechanisms in hypertensive models; leaves open human translation.
Elevated whole blood viscosity can significantly contribute to an increase in total peripheral resistance, disruption of systemic hemodynamics, and development of microcirculatory disorders in arterial hypertension. Meanwhile, changes in blood viscosity (BV) also lead to changes in endothelial shear stress, which can affect vascular tone. Studies of the correlation between changes in BV and blood pressure in animals under conditions of arterial hypertension have not been conducted. This work was aimed to bridge this gap using normotensive Wistar rats and spontaneously hypertensive rats (SHR) in norm, as well as under conditions of decreased and increased BV. BV was decreased/increased via isovolumic hemodilution/hemoconcentration. Mean arterial pressure (MAP) was recorded using a Biopac MP150 system (USA). BV was measured by a Brookfield DV–II+ Pro rotational viscometer (USA) at a shear rate of 450 s–1. Normotensive rats demonstrated no statistically significant correlations between BV and MAP baseline values. After isovolumic hemodilution or hemoconcentration in normotensive rats, a statistically significant BV–MAP relationship was also not found. In SHR, as compared to Wistar rats, a significant moderate positive correlation was revealed between BV and MAP baseline values (R = 0.643, p < 0.05), persisting after both hemodilution (R = 0.530, p < 0.05) and hemoconcentration (R = 0.689, p < 0.05). A correlation analysis shows that in SHR, unlike Wistar rats, changes in MAP passively follow those in BV, which is probably due to a failure of the mechanisms of endothelium-dependent vasodilation in arterial hypertension.
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Анищенко et al. (2024) studied this question.
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