Effects of interactions in natural gas/water/rock system on hydrocarbon migration and accumulation

The study of natural gas accumulation process in tight formation has become the focus of the petroleum industry. One of the priorities is the effects of interactions in natural gas/water/rock system on hydrocarbon migration and accumulation process. On the macroscopic scale, we investigate the interactions in natural gas/water/rock system by formation fluorescence test and production data analysis. One the microscopic scale, the mechanisms are revealed by mathematical analysis and experimental methods considering the variation of geological temperature and pressure. The effects of interactions in natural gas/water/rock system are also simulated by numerical simulation. The results are visualized and quantified. A novel semi-analytical method based on a physical experiment is proposed to calculate the temperature- and pressure-dependent contact angle and interface tension which reflect the interactions in the natural gas–water–rock system. This semi-analytical is embedded in the numerical simulation during the simulation of the natural gas charging process. The results indicate that with the increase of geological temperature and pressure, the contact angle will increase and the interface tension between natural gas and water will decrease. The capillary resistance in the formation will be reduced. Since the decrease of capillary resistance, the natural gas can be charged into smaller pores, so that the actual charging threshold is lower than the one originally obtained under present reservoir conditions. After considering the temperature and pressure during the accumulation process, some sand bodies that were thought not to be charged may have natural gas accumulate.

Distribution of Flow in an Arteriovenous Fistula Using Reduced-order Models

The creation of a communication between an artery and a vein (arteriovenous fistula or AVF), to speed up the blood purification during hemodialysis of patients with renal insufficiency, induces significant rheological and mechanical modifications of the vascular network. In this study, we investigated the impact of the creation of an AVF with a zero-dimensional network model of the vascular system of an upper limb and a one-dimensional model around the anastomosis. We compared the simulated distribution of flow rate in this vascular system with Doppler ultrasound measurements. We studied three configurations: before the creation of the AVF, after the creation of the AVF, and after a focal reduction due to a hyper flow rate. The 0D model predicted the bounds of the diameter of the superficial vein that respects the flow constraints, assuming a high capillary resistance. We indeed highlighted the importance of knowing the capillary resistance as it is a decisive parameter in the models. We also found that the model reproduced the Doppler measurements of flow rate in every configuration and predicted the distribution of flow in cases where the Doppler was not available. The 1D model allowed studying the impact of a venous constriction on the flow distribution, and the capillary resistance was still a crucial parameter.

Coronary capillary blood flow in a rat model of congestive heart failure

The aim of this study was to explore the role of abnormal coronary microvasculature morphology and hemodynamics in the development of congestive heart failure (CHF). CHF was induced in rats by aortic banding, followed by ischemia-reperfusion and later aortic debanding. Polymerized casts of coronary vasculature were imaged under a scanning electron microscope (SEM). Matrix Laboratory (MATLAB) software was used to calculate capillary structure index (CSI), a measure of structural alignment also called mean vector length (MVL), for 93 SEM images of coronary capillaries (CSI→1 perfect linearity; CSI→0 circular disarray). CSI was incorporated as a constant to represent tortuosity and nonlaminar flow in Poiseuille’s equation to estimate the differences in capillary blood flow rate, velocity, and resistance for CHF vs. control. The morphology of CHF capillaries is significantly disordered and tortuous compared with control (CSI: 0.35 ± 0.02 for 61 images from 7 CHF rats; 0.58 ± 0.02 for 32 images from 7 control rats; P < 0.01). Estimated capillary resistance in CHF is elevated by 173% relative to control, while blood flow rate and blood velocity are 56 and 43% slower than control. Capillary resistance increased 67% due to the significantly narrower capillary diameter in CHF, while it increased an additional 105% due to tortuosity. The significant structural abnormalities of CHF coronary capillaries may drastically stagnate hemodynamics in myocardium and increase resistance to blood flow. This could play a role in the development of CHF.NEW & NOTEWORTHY In the present study, coronary capillary tortuosity was measured by applying Matrix Laboratory software to scanning electron microscope images of capillaries in a rat model of congestive heart failure. Stagnant blood flow in coronary capillaries may play a role in the development of congestive heart failure. The application of computer modeling to histological and physiological data to characterize the hemodynamics of coronary microcirculation is a new area of study.

Bioinspired surfaces for turbulent drag reduction

In this review, we discuss how superhydrophobic surfaces (SHSs) can provide friction drag reduction in turbulent flow. Whereas biomimetic SHSs are known to reduce drag in laminar flow, turbulence adds many new challenges. We first provide an overview on designing SHSs, and how these surfaces can cause slip in the laminar regime. We then discuss recent studies evaluating drag on SHSs in turbulent flow, both computationally and experimentally. The effects of streamwise and spanwise slip for canonical, structured surfaces are well characterized by direct numerical simulations, and several experimental studies have validated these results. However, the complex and hierarchical textures of scalable SHSs that can be applied over large areas generate additional complications. Many studies on such surfaces have measured no drag reduction, or even a drag increase in turbulent flow. We discuss how surface wettability, roughness effects and some newly found scaling laws can help explain these varied results. Overall, we discuss how, to effectively reduce drag in turbulent flow, an SHS should have: preferentially streamwise-aligned features to enhance favourable slip, a capillary resistance of the order of megapascals, and a roughness no larger than 0.5, when non-dimensionalized by the viscous length scale. This article is part of the themed issue ‘Bioinspired hierarchically structured surfaces for green science’.

Shedding of the endothelial glycocalyx in arterioles, capillaries, and venules and its effect on capillary hemodynamics during inflammation

The endothelial glycocalyx has been identified as a barrier to transvascular exchange of fluid, macromolecules, and leukocyte-endothelium [endothelial cell (EC)] adhesion during the inflammatory process. Shedding of glycans and structural changes of the glycocalyx have been shown to occur in response to several agonists. To elucidate the effects of glycan shedding on microvascular hemodynamics and capillary resistance to flow, glycan shedding in microvessels in mesentery (rat) was induced by superfusion with 10−7M fMLP. Shedding was quantified by reductions of fluorescently labeled lectin (BS-1) bound to the EC and reductions in thickness of the barrier to infiltration of 70-kDa dextran on the EC surface. Red cell velocities (two-slit technique), pressure drops (dual servo-null method), and capillary hematocrit (direct cell counting) were measured in parallel experiments. The results indicate that fMLP caused shedding of glycans in all microvessels with reductions in thickness of the barrier to 70-kDa dextran of 110, 80, and 123 nm, in arterioles, capillaries, and venules, respectively. Intravascular volumetric flows fell proportionately in all three divisions in response to rapid obstruction of venules by white blood cell (WBC)-EC adhesion, and capillary resistance to flow rose 18% due to diminished deformability of activated WBCs. Capillary resistance fell significantly 26% over a 30-min period, as glycans were shed from the EC surface to increase effective capillary diameter, whereas capillary hematocrit and anatomic diameter remained invariant. This decrease in capillary resistance mitigates the increase in resistance due to diminished WBC deformability, and hence these concurrent rheological events may be of equal importance in affecting capillary flow during the inflammatory process.