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Numerical simulation of effect of hybrid nanofluid on heat transfer and flow of the Newtonian pulsatile blood through 3D occluded artery: Silver and gold nanoparticles

Koosha N, Mosavi V, Kheirollah J, Najafi N, Abdi N, Alizadeh A, et al.

J Therm Biol, 2023 Oct;117:103718.
PMID: 37812951 DOI: 10.1016/j.jtherbio.2023.103718

The study of blood flow in obstructed arteries is a significant focus in computational fluid dynamics, particularly in the field of biomedicine. The primary objective of this research is to investigate the impact of pulsating blood velocity on heat transfer within biological systems, with a specific focus on blood flow in obstructed arteries. To achieve this goal, a comprehensive 3D model representing a straight, constricted blood vessel has been developed. This model incorporates periodic, unsteady, Newtonian blood flow along with the presence of gold and silver nanoparticles. Leveraging the Finite Element Method (FEM), the Navier-Stokes and energy equations have been rigorously solved. Through the investigation, it is aim to shed light on how alterations in the pulsation rate and the volume fraction of nanoparticles influence both temperature distribution and velocity profiles within the system. The present study findings unequivocally highlight that the behavior of pulsatile nanofluid flow significantly impacts the velocity field and heat transfer performance. However, it is imperative to note that the extent of this influence varies depending on the specific volume fractions involved. Specifically, higher volume fractions of nanofluids correlate with elevated velocities at the center of the vessel and decreased velocities near the vessel walls. This pattern also extends to the temperature distribution and heat flux within the vessel, further underscoring the paramount importance of pulsatile flow dynamics in biomedicine and computational fluid dynamics research. Besides, results revealed that the presence of occlusion significantly affects the heat transfer and fluid flow.

Matched MeSH terms: Arteries/physiology
Method optimization to assess endothelial function in females-duration of glyceryl trinitrate effect

Ibrahim NN, Rasool AH, Wong AR, Rahman AR

Methods Find Exp Clin Pharmacol, 2007 Jun;29(5):349-52.
PMID: 17805437

Pulse-wave analysis (PWA) combined with pharmacological challenges has recently been used as a method to measure endothelial function. This involved administration of glyceryl trinitrate (GTN), followed by salbutamol as endothelium-independent and -dependent vasodilators, respectively. The duration of GTN effect needs to be established before the administration of salbutamol. Baseline augmentation index (AIx) and pulse-wave velocity (PWV) measurements were taken in 11 healthy female subjects (mean age 23.27 +/- 3.66 years). Sublingual GTN 0.5 mg was administered for 3 min, followed by AIx and PWV measurements every 5 min till 20 min and then every 10 min until 40 min post-GTN. Maximum change in AIx post-GTN was at 3 min with a mean change from the baseline of -17.86% +/- 4.40% (p < 0.001). There were no significant changes noted after 30 and 40 min with mean change being -0.82% +/- 2.61% and 0.14% +/- 3.20%, respectively (p > 0.05). Significant changes in PWV were noted at 5 and 10 min with the mean change of -0.33 +/- 0.36 m/s and -0.33 +/- 0.35 m/s, respectively (p = 0.01). There were no further changes noted at 15 min and thereafter (p > 0.05). A duration of at least 30 min after GTN is required for AIx and PWV values to reach their baseline. Thus, the administration of salbutamol should be given only after 30 min of sublingual GTN for the assessment of endothelial function.

Matched MeSH terms: Carotid Arteries/physiology*
Characterization of a novel tetrandrine-induced contraction in rat tail artery

Achike FI, Kwan CY

Acta Pharmacol Sin, 2002 Aug;23(8):698-704.
PMID: 12147191

In an attempt to pharmacologically characterize the Chinese antihypertensive drug, tetrandrine, we observed in rat-tail arteries, an unusual contraction in tissues that were stimulated with high [KCl] and not those stimulated with phenylephrine. The characteristics of this contraction were studied.

Matched MeSH terms: Arteries/physiology
Vitamin E and its effect on arterial stiffness in postmenopausal women--a randomized controlled trial

Rasool AH, Rehman A, Wan Yusuf WN, Rahman AR

Int J Clin Pharmacol Ther, 2003 Dec;41(12):587-92.
PMID: 14692708

INTRODUCTION: Arterial stiffness is emerging as a useful index of vascular health. Postmenopausal women have been shown to have stiffer arteries. Hormone replacement therapy and soy isoflavones improve arterial stiffness in these women. The aim of this study is to establish whether vitamin E improves arterial stiffness in postmenopausal women after 10 weeks of supplementation.
METHODS: Twenty postmenopausal women with a mean age of 54.59 +/- 1.22 years participated in this randomized, crossover, double-blind, placebo-controlled clinical trial. All women received 400 IU of tocopherol daily for 10 weeks or a placebo capsule, before being crossed over for treatment. At intervals of 5 weeks, subjects attended sessions where measurements of arterial stiffness, blood pressure and plasma vitamin E level were taken. Pulse wave velocity measurement, using the automated Complior machine, was used as an index of arterial stiffness.
RESULTS: Plasma vitamin E level was 30.38 +/- 1.56 micromol/l at baseline, after treatment it was 59.01 +/- 3.30 micromol/l and 31.17 +/- 1.37 micromol/l with vitamin E and placebo, respectively (p < 0.001). There was no significant difference in pulse wave velocity after 10-week treatment with placebo and vitamin E (9.14 +/- 0.29 versus 9.04 +/- 0.29 m/s, respectively). Similarly, no difference in systolic and diastolic blood pressure was seen between placebo and vitamin E at the end of 10 weeks.
CONCLUSION: Supplementary vitamin E for 10 weeks at 400 IU daily has no effect on arterial stiffness in healthy postmenopausal women.

Matched MeSH terms: Arteries/physiology*
Fulltext "A Step and a Ceiling": mechanical properties of Ca2+ spark vasoregulation in resistance arteries by pressure-induced oxidative activation of PKG

Csato V, Kadir SZSA, Khavandi K, Bennett H, Sugden S, Gurney AM, et al.

Physiol Rep, 2019 Nov;7(22):e14260.
PMID: 31782255 DOI: 10.14814/phy2.14260

We investigated the biomechanical relationship between intraluminal pressure within small mesenteric resistance arteries, oxidant activation of PKG, Ca2+ sparks, and BK channel vasoregulation. Mesenteric resistance arteries from wild type (WT) and genetically modified mice with PKG resistance to oxidative activation were studied using wire and pressure myography. Ca2+ sparks and Ca2+ transients within vascular smooth muscle cells of intact arteries were characterized using high-speed confocal microscopy of intact arteries. Arteries were studied under conditions of varying intraluminal pressure and oxidation. Intraluminal pressure specifically, rather than the generic stretch of the artery, was necessary to activate the oxidative pathway. We demonstrated a graded step activation profile for the generation of Ca2+ sparks and also a functional "ceiling" for this pressure --sensitive oxidative pathway. During steady state pressure - induced constriction, any additional Ca2+ sensitive-K+ channel functional availability was independent of oxidant activated PKG. There was an increase in the amplitude, but not the Area under the Curve (AUC) of the caffeine-induced Ca2+ transient in pressurized arteries from mice with oxidant-resistant PKG compared with wild type. Overall, we surmise that intraluminal pressure within resistance arteries controls Ca2+ spark vasoregulation through a tightly controlled pathway with a graded onset switch. The pathway, underpinned by oxidant activation of PKG, cannot be further boosted by additional pressure or oxidation once active. We propose that these restrictive characteristics of pressure-induced Ca2+ spark vasoregulation confer stability for the artery in order to provide a constant flow independent of additional pressure fluctuations or exogenous oxidants.

Matched MeSH terms: Mesenteric Arteries/physiology*