Computational fluid dynamic simulation of two-fluid non-Newtonian nanohemodynamics through a diseased artery with a stenosis and aneurysm.

This article presents a two-dimensional theoretical study of hemodynamics through a diseased permeable artery with a mild stenosis and an aneurysm present. The effect of metallic nanoparticles on the blood flow is considered, motivated by drug delivery (pharmacology) applications. Two different models are adopted to mimic non-Newtonian characteristics of the blood flow; the Casson (viscoplastic) fluid model is deployed in the core region and the Sisko (viscoelastic) fluid model employed in the peripheral (porous) region. The revised Buongiorno two-component nanofluid model is utilized for nanoscale effects. The blood is considered to contain a homogenous suspension of nanoparticles. The governing equations are derived by extending the Navier-Stokes equations with linear Boussinesq approximation (which simulates both heat and mass transfer). Natural (free) double-diffusive convection is considered to simulate the dual influence of thermal and solutal buoyancy forces. The conservation equations are normalised by employing appropriate non-dimensional variables. The transformed equations are solved numerically using the finite element method with the variational formulation scheme available in the FreeFEM++ code. A comprehensive mesh-independence study is included. The effect of selected parameters (thermophoresis, Brownian motion, Grashof number, thermo-solutal buoyancy ratio, Sisko parameter ratio, and permeability parameter) on velocity, temperature, nanoparticle concentration, and hemodynamic pressure have been calculated for two clinically important cases of arteries with stenosis and an aneurysm. Skin-friction coefficient, Nusselt number, volumetric flow rate, and resistance impedance of blood flow are also computed. Colour contours and graphs are employed to visualize the simulated blood flow characteristics. It is observed that by increasing the thermal buoyancy parameter, i.e. Grashof number (Gr), the nanoparticle concentration and temperature decrease, whereas velocity increases with an increment in the Brownian motion parameter (Nb). Furthermore, velocity decreases in the peripheral porous region with elevation in the Sisko material ratio (m) and permeability parameter (k'). The simulations are relevant to transport phenomena in pharmacology and nano-drug targeted delivery in haematology.

Inhibition of Angiotensin-II Production Increases Susceptibility to Acute Ischemia/Reperfusion Arrhythmia.

BACKGROUND Myocardial ischemia and reperfusion lead to impairment of electrolyte balance and, eventually, lethal arrhythmias. The aim of this study was to investigate the effects of pharmacological inhibition of angiotensin-II (Ang-II) production on heart tissue with ischemia-reperfusion damage, arrhythmia, and oxidative stress. MATERIAL AND METHODS Rats were divided into 4 groups: only ischemia/reperfusion (MI/R), captopril (CAP), aliskiren (AL), and CAP+AL. The drugs were given by gavage 30 min before anesthesia. Blood pressure and electrocardiography (ECG) were recorded during MI/R procedures. The heart tissue and plasma was kept so as to evaluate the total oxidant (TOS), antioxidant status (TAS), and creatine kinase-MB (CK-MB). RESULTS Creatine kinase-MB was not different among the groups. Although TAS was not affected by inhibition of Ang-II production, TOS was significantly lower in the CAP and/or AL groups than in the MI/R group. Furthermore, oxidative stress index was significantly attenuated in the CAP and/or AL groups. Captopril significantly increased the duration of VT during ischemia; however, it did not have any effect on the incidence of arrhythmias. During reperfusion periods, aliskiren and its combinations with captopril significantly reduced the incidence of other types of arrhythmias. Captopril alone had no effect on the incidence of arrhythmias, but significantly increased arrhythmias score and durations of arrhythmias during reperfusion. MAP and heart rate did not show changes in any groups during ischemic and reperfusion periods. CONCLUSIONS Angiotensin-II production appears to be associated with elevated levels of reactive oxygen species, but Ang-II inhibitions increases arrhythmia, mainly by initiating ventricular ectopic beats.