Computational simulations suggest that microvascular rarefaction, not inward eutrophic remodeling, primarily drives the reduction in vascular flow reserve seen in hypertension.
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Rarefaction may drive hypertensive flow reserve loss in models; challenges remodeling hypotheses and leaves open human validation.
Vascular flow reserve (VFR) is the relative increase in tissue perfusion from the resting state to a state with maximum vasodilatation. Longstanding hypertension reduces the VFR, which in turn reduces the maximum working capacity of the tissue. In principle, both inward arteriolar remodelling and rarefaction of the microvascular network may contribute to this reduction. These processes are known to occur simultaneously in the microcirculation of the hypertensive individual and both cause a reduction in the luminal trans-sectional area available for perfusion. Which of them is the main factor responsible for the reduction in VFR is, however, not known. Here we present simulations performed on large microvascular networks to assess the VFR in various situations. Particular attention is paid to the VFR in networks in which the vessels have structurally adapted to a sustained increase in pressure by inward eutrophic remodelling (IER), i.e. by redistributing the same amount of wall material around a smaller lumen. Collectively, the results indicate that the IER may not per se be the main factor responsible for the hypertensive reduction in VFR. Rather, it may be explained by the presence of arteriolar and capillary rarefaction.
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Jacobsen et al. (2010) studied this question.
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