The hematocrit is normally between 0.40-0.51 in men and 0.36-0.47 in women. Exercise, arousal, food ingestion, hypoxia (for example breath holding), bleeding, and injection of catecholamines quickly increases the hematocrit, partly because of contraction of the spleen. Long-term hematocrit is regulated by peritubular fibroblasts of the renal cortex which produce erythropoietin (EPO) in response to hypoxia; EPO stimulates the production of red blood cells in the bone marrow.
In analysis of PET studies, hematocrit is often needed in conversion of blood radioactivity concentrations to plasma concentrations, and vice versa. In heart chambers the hematocrit is the same as in venous blood samples (Brudin et al., 1986).
Hematocrit is usually lower in the smaller vessels in tissue than in the large veins or arteries from where the blood samples are withdrawn. The spleen is an exception; hematocrit in splenic blood is usually almost two times higher than in arterial blood. Otherwise, microvessel haematocrit may be less than half of the systemic haematocrit. In microvessels with diameter <100 µm the RBC velocity is higher than the velocity of plasma (Fahraeus, 1928); in addition to this vessel Fahraeus effect, the heterogeneity of blood velocity leads to network Fahraeus effect. It should be noted that Fahraues effect does not affect to the O2 delivery to the tissue, because that is dependent on the flow fraction of RBCs, which in practise is the same as the HCT in larger vessels (Pries et al., 1986). Yet, short capillary transit time may limit O2 diffusion, because oxygen in RBC does not equilibrate with tissue, at least in working muscle (Honig & Gayeski, 1993). Conditions that elevate skeletal muscle blood flow increase capillary HCT, increasing RBC surface area-to-capillary luminal surface area, which augments O2 diffusing capacity (Kindig et al., 2002).
Labelled human serum albumin ([62Cu]-HSA-DTS, [62Cu]-NEB, [18F]-AlF-NEB, [methyl-11C]albumin, etc), can be used as a plasma-pool imaging agent, and oxygen-15 labelled carbon monoxide, [15O]CO, as a erythrocyte imaging agent. Together these PET tracers can be used to determine the regional hematocrit and regional/large-vessel hematocrit ratio.
Mean regional cerebral hematocrit was 38.3 ± 3.45 % in 12 normal volunteers, and mean cerebral/large-vessel hematocrit ratio was 0.88 ± 0.06 (Okazawa et al. 1996). In the same study, in patients with cerebrovascular disease, regional cerebral hematocrit was significantly lower.
This cerebral/large-vessel hematocrit ratio is close to the value 0.85 (Grubb et al. 1973), which is used widely in the literature (Phelps et al., 1979), for example, in determination of the blood volume using [15O]CO PET, but clearly higher than the value 0.69 determined from nine subjects using [11C]methyl-albumin and [11C]CO (Lammertsma et al. 1984; Brooks et al., 1986). Calamante et al. (2016) applied a MRI-based method that also provided similar value of 0.88 for the cerebral/arterial ratio, and 0.86 for cortical- and sub-cortical regions.
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Calamante F, Ahlgren A, van Osch MJP, Knutsson L. A novel approach to measure local cerebral haematocrit using MRI. J Cereb Blood Flow Metab. 2016; 36(4): 768-780. doi: 10.1177/0271678X15606143.
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Okazawa H, Yonekura Y, Fujibayashi Y, Yamauchi H, Ishizu K, Nishizawa S, Magata Y, Tamaki N, Fukuyama H, Yokoyama A, Konishi J. Measurement of regional cerebral plasma pool and hematocrit with copper-62-labeled HSA-DTS. J Nucl Med 1996; 37: 1080-1085.
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Updated at: 2019-09-25
Created at: 2008-03-27
Written by: Vesa Oikonen