Dataset Information

Observation of natural flexural pulse waves in retinal and carotid arteries for wall elasticity estimation.

ABSTRACT: The risk of cardiovascular events is linked to arterial elasticity that can be estimated from the pulse wave velocity. This symmetric wave velocity is related to the wall elasticity through the Moens-Korteweg equation. However, ultrasound imaging techniques need improved accuracy, and optical measurements on retinal arteries produce inconsistent results. Here, we report the first observation of an antisymmetric pulse wave: the flexural pulse wave. An optical system performs in vivo wave velocity measurements on retinal arteries and veins. Velocity estimation ranges between 1 and 10 millimeter per second. The theory of guided waves confirms the existence of this wave mode and its low velocity. Natural flexural waves can also be detected at the bigger scale of a carotid artery using ultrafast ultrasound imaging. This second natural pulse wave has great potential of becoming a biomarker of blood vessel aging.

SUBMITTER: Laloy-Borgna G

PROVIDER: S-EPMC10284541 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature

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Observation of natural flexural pulse waves in retinal and carotid arteries for wall elasticity estimation.

Laloy-Borgna Gabrielle G Puyo Léo L Nishino Hidero H Atlan Michael M Catheline Stefan S

Science advances 20230621 25

The risk of cardiovascular events is linked to arterial elasticity that can be estimated from the pulse wave velocity. This symmetric wave velocity is related to the wall elasticity through the Moens-Korteweg equation. However, ultrasound imaging techniques need improved accuracy, and optical measurements on retinal arteries produce inconsistent results. Here, we report the first observation of an antisymmetric pulse wave: the flexural pulse wave. An optical system performs in vivo wave velocity ...[more]

PMID: 37343110

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Project description:PurposeThe purpose of the study was to describe ocular blood flow changes in eyes affected by a carotid-cavernous fistula (CCF) using laser speckle flowgraphy. We hypothesized that imaging blood flow velocity waveforms in the retinal arterioles and venules simultaneously would reveal specific characteristics of an arteriovenous (AV) connection.DesignThe study was an observational case series, with a retrospective case-control analysis.MethodsFive patients with a CCF underwent measurement of ocular blood flow using laser speckle flowgraphy. The blood flow was compared retrospectively between a control group of healthy subjects (n = 32) and patients with an elevated intraocular pressure or venous outflow impairment without an AV fistula (n = 40). The outcomes were derived from the arteriole and venule blood flow velocity waveforms, including an A-V phase delay and flow pulsatility.ResultsThe presence of an active CCF was associated with an increased delay in the peak velocity measured in the retinal venule (10.7% ± 2.2% of the cardiac cycle duration) compared with unaffected fellow eyes (1.8% ± 0.2%; p = 0.05) or control eyes of normal subjects (2.7% ± 0.3%; p = 0.02). This delay disappeared after fistula thrombosis and was not present in eyes with a central retinal vein occlusion (CRVO), glaucoma, non-arteritic anterior ischemic optic neuropathy (NAION), or papilledema. The venule blood flow velocity decreased during systole (and in some cases momentarily stopped), leading to a delayed pulse with a greater amplitude in the venules than in fellow eyes and normal controls after normalizing to the arteriole amplitude (1.71 ± 0.3 vs 0.54 ± 0.03 vs 0.59 ± 0.02; p = 8.0E-12). This specific AV delay could also be identified in a scanning laser ophthalmoscope (SLO; SPECTRALIS®) video.ConclusionLaser speckle flowgraphy reveals dynamic retinal vascular changes in eyes affected by a CCF, which are not present in healthy controls or patients with other eye conditions, and which reverses with treatment.

Project description:UnlabelledThe fungal cell wall confers cell morphology and protection against environmental insults. For fungal pathogens, the cell wall is a key immunological modulator and an ideal therapeutic target. Yeast cell walls possess an inner matrix of interlinked β-glucan and chitin that is thought to provide tensile strength and rigidity. Yeast cells remodel their walls over time in response to environmental change, a process controlled by evolutionarily conserved stress (Hog1) and cell integrity (Mkc1, Cek1) signaling pathways. These mitogen-activated protein kinase (MAPK) pathways modulate cell wall gene expression, leading to the construction of a new, modified cell wall. We show that the cell wall is not rigid but elastic, displaying rapid structural realignments that impact survival following osmotic shock. Lactate-grown Candida albicans cells are more resistant to hyperosmotic shock than glucose-grown cells. We show that this elevated resistance is not dependent on Hog1 or Mkc1 signaling and that most cell death occurs within 10 min of osmotic shock. Sudden decreases in cell volume drive rapid increases in cell wall thickness. The elevated stress resistance of lactate-grown cells correlates with reduced cell wall elasticity, reflected in slower changes in cell volume following hyperosmotic shock. The cell wall elasticity of lactate-grown cells is increased by a triple mutation that inactivates the Crh family of cell wall cross-linking enzymes, leading to increased sensitivity to hyperosmotic shock. Overexpressing Crh family members in glucose-grown cells reduces cell wall elasticity, providing partial protection against hyperosmotic shock. These changes correlate with structural realignment of the cell wall and with the ability of cells to withstand osmotic shock.ImportanceThe C. albicans cell wall is the first line of defense against external insults, the site of immune recognition by the host, and an attractive target for antifungal therapy. Its tensile strength is conferred by a network of cell wall polysaccharides, which are remodeled in response to growth conditions and environmental stress. However, little is known about how cell wall elasticity is regulated and how it affects adaptation to stresses such as sudden changes in osmolarity. We show that elasticity is critical for survival under conditions of osmotic shock, before stress signaling pathways have time to induce gene expression and drive glycerol accumulation. Critical cell wall remodeling enzymes control cell wall flexibility, and its regulation is strongly dependent on host nutritional inputs. We also demonstrate an entirely new level of cell wall dynamism, where significant architectural changes and structural realignment occur within seconds of an osmotic shock.

Dataset Information

Observation of natural flexural pulse waves in retinal and carotid arteries for wall elasticity estimation.

Publications

Observation of natural flexural pulse waves in retinal and carotid arteries for wall elasticity estimation.

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