The volume of healthy red blood cells is optimal for advective oxygen transport in arterioles

Amoudruz, Lucas; Economides, Athena; Koumoutsakos, Petros

doi:10.1016/j.bpj.2024.04.015

Cited by 3 publications

References 47 publications

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Intestinal oxygen utilisation and cellular adaptation during intestinal ischaemia–reperfusion injury

Archontakis‐Barakakis,

Mavridis,

Chlorogiannis

et al. 2024

Clinical & Translational Med

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The gastrointestinal tract can be deranged by ailments including sepsis, trauma and haemorrhage. Ischaemic injury provokes a common constellation of microscopic and macroscopic changes that, together with the paradoxical exacerbation of cellular dysfunction and death following restoration of blood flow, are collectively known as ischaemia–reperfusion injury (IRI). Although much of the gastrointestinal tract is normally hypoxemic, intestinal IRI results when there is inadequate oxygen availability due to poor supply (pathological hypoxia) or abnormal tissue oxygen use and metabolism (dysoxia). Intestinal oxygen uptake usually remains constant over a wide range of blood flows and pressures, with cellular function being substantively compromised when ischaemia leads to a >50% decline in intestinal oxygen consumption. Restoration of perfusion and oxygenation provokes additional injury, resulting in mucosal damage and disruption of intestinal barrier function. The primary cellular mechanism for sensing hypoxia and for activating a cascade of cellular responses to mitigate the injury is a family of heterodimer proteins called hypoxia‐inducible factors (HIFs). The HIF system is connected to numerous biochemical and immunologic pathways induced by IRI and the concentration of those proteins increases during hypoxia and dysoxia. Activation of the HIF system leads to augmented transcription of specific genes in various types of affected cells, but may also augment apoptotic and inflammatory processes, thus aggravating gut injury.Key points During intestinal ischaemia, mitochondrial oxygen uptake is reduced when cellular oxygen partial pressure decreases to below the threshold required to maintain normal oxidative metabolism. Upon reperfusion, intestinal hypoxia may persist because microcirculatory flow remains impaired and/or because available oxygen is consumed by enzymes, intestinal cells and neutrophils.

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Intestinal oxygen utilisation and cellular adaptation during intestinal ischaemia–reperfusion injury

Archontakis‐Barakakis,

Mavridis,

Chlorogiannis

et al. 2024

Clinical & Translational Med

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Unsteady solute dispersion in large arteries under periodic body acceleration

Das,

Mahata,

Patne

et al. 2024

Physics of Fluids

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The present study investigates the effect of periodic body acceleration on solute dispersion in blood flow through large arteries. Transport coefficients (i.e., exchange, convection, and dispersion coefficients) and mean concentration of the solute are analyzed in the presence of wall absorption. The solute is quickly transported to the wall of arteries with a smaller radius, whereas the opposite is true for arteries with a larger radius. In the presence of body acceleration, the amplitude of fluctuations of the convection coefficient K1(t) increases significantly as the radius of the artery increases. In contrast, an opposite scenario exists for the dispersion coefficient K2(t). The solute dispersion process becomes more effective in arterial blood flow as the radius of the artery decreases. More interestingly, in large arteries with body acceleration, the solute is convected, dispersed, and distributed more toward the upstream direction owing to flow reversal during the diastolic phase of pressure pulsation. Note that this important feature of flow reversal is solely due to periodic body acceleration. For an artery with a small radius, under the influence of periodic body acceleration, the mean concentration of solute Cm is the minimum, and more axial spread is noticed in the axial direction. In contrast, an opposite scenario arises in the artery with a large radius. Additionally, the effect of body acceleration on the shear-induced diffusion of red blood cells is discussed in blood flow.

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Noisy hemoglobin consumption by erythrocyticPlasmodium falciparumparasites: origins and possible implications

Perko,

Singh,

Lopez

et al. 2024

Preprint

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Non-genetic cell-to-cell phenotypic differences can significantly impact pathogen physiology and virulence, leading to unexpected phenomena such as antibiotic persistence. Here, we introduce the role of such non-genetic phenotypic differences in the host, with a focus on hemoglobin consumption by Plasmodium falciparum during the erythrocytic stage of parasite development. Through imaging, we quantified the substantial variability in hemoglobin (Hb) concentration among uninfected red blood cells (RBCs), and subsequently measured the rate of Hb consumption by parasites at different stages of their life cycle. This revealed a similarly significant variability among different infected RBCs. By employing a mathematical model, we demonstrated that this variability in Hb consumption can be attributed to non-genetic differences in host RBCs, marking the first evidence of this phenomenon in malaria parasite physiology. These findings underscore the importance of incorporating non-genetic host variability into models of disease progression and treatment strategies for malaria and potentially other pathogen-related diseases.

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The volume of healthy red blood cells is optimal for advective oxygen transport in arterioles

Cited by 3 publications

References 47 publications

Intestinal oxygen utilisation and cellular adaptation during intestinal ischaemia–reperfusion injury

Intestinal oxygen utilisation and cellular adaptation during intestinal ischaemia–reperfusion injury

Unsteady solute dispersion in large arteries under periodic body acceleration

Noisy hemoglobin consumption by erythrocyticPlasmodium falciparumparasites: origins and possible implications

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