Pulsatile Nature Research Articles

Numerical simulation of the non-Newtonian blood flow through a mechanical aortic valve

This work focuses on the comparison between Newtonian and non-Newtonian blood flows through a bileaflet mechanical heart valve in the aortic root. The blood, in fact, is a concentrated suspension of cells, mainly red blood cells, in a Newtonian matrix, the plasma, and consequently its overall behavior is that of a non-Newtonian fluid owing to the action of the cells’ membrane on the fluid part. The common practice, however, assumes the blood in large vessels as a Newtonian fluid since the shear rate is generally high and the effective viscosity becomes independent of the former. In this paper, we show that this is not always the case even in the aorta, the largest artery of the systemic circulation, owing to the pulsatile and transitional nature of the flow. Unexpectedly, for most of the pulsating cycle and in a large part of the fluid volume, the shear rate is smaller than the threshold level for the blood to display a constant effective viscosity and its shear thinning character might affect the system dynamics. A direct inspection of the various flow features has shown that the valve dynamics, the transvalvular pressure drop and the large-scale features of the flow are very similar for the Newtonian and non-Newtonian fluid models. On the other hand, the mechanical damage of the red blood cells (hemolysis), induced by the altered stress values in the flow, is larger for the non-Newtonian fluid model than for the Newtonian one.

Mechanical stretch: physiological and pathological implications for human vascular endothelial cells.

Vascular endothelial cells are subjected to hemodynamic forces such as mechanical stretch due to the pulsatile nature of blood flow. Mechanical stretch of different intensities is detected by mechanoreceptors on the cell surface which enables the conversion of external mechanical stimuli to biochemical signals in the cell, activating downstream signaling pathways. This activation may vary depending on whether the cell is exposed to physiological or pathological stretch intensities. Substantial stretch associated with normal physiological functioning is important in maintaining vascular homeostasis as it is involved in the regulation of cell structure, vascular angiogenesis, proliferation and control of vascular tone. However, the elevated pressure that occurs with hypertension exposes cells to excessive mechanical load, and this may lead to pathological consequences through the formation of reactive oxygen species, inflammation and/or apoptosis. These processes are activated by downstream signaling through various pathways that determine the fate of cells. Identification of the proteins involved in these processes may help elucidate novel mechanisms involved in vascular disease associated with pathological mechanical stretch and could provide new insight into therapeutic strategies aimed at countering the mechanisms’ negative effects.

Variability in vascular smooth muscle cell stretch-induced responses in 2D culture.

The pulsatile nature of blood flow exposes vascular smooth muscle cells (VSMCs) in the vessel wall to mechanical stress, in the form of circumferential and longitudinal stretch. Cyclic stretch evokes VSMC proliferation, apoptosis, phenotypic switching, migration, alignment, and vascular remodeling. Given that these responses have been observed in many cardiovascular diseases, a defined understanding of their underlying mechanisms may provide critical insight into the pathophysiology of cardiovascular derangements. Cyclic stretch-triggered VSMC responses and their effector mechanisms have been studied in vitro using tension systems that apply either uniaxial or equibiaxial stretch to cells grown on an elastomer-bottomed culture plate and ex vivo by stretching whole vein segments with small weights. This review will focus mainly on VSMC responses to the in vitro application of mechanical stress, outlining the inconsistencies in acquired data, and comparing them to in vivo or ex vivo findings. Major discrepancies in data have been seen in mechanical stress-induced proliferation, apoptosis, and phenotypic switching responses, depending on the stretch conditions. These discrepancies stem from variations in stretch conditions such as degree, axis, duration, and frequency of stretch, wave function, membrane coating, cell type, cell passage number, culture media content, and choice of in vitro model. Further knowledge into the variables that cause these incongruities will allow for improvement of the in vitro application of cyclic stretch.

60 YEARS OF NEUROENDOCRINOLOGY: The posterior pituitary, from Geoffrey Harris to our present understanding.

Geoffrey Harris pioneered our understanding of the posterior pituitary, mainly with experiments that involved the electrical stimulation of the supraoptico-hypophysial tract. In the present essay, we explain how his observations included clues to the pulsatile nature of the oxytocin signal - clues that were followed up by subsequent workers, including his students and their students. These studies ultimately led to our present understanding of the milk-ejection reflex and of the role of oxytocin in parturition. Discoveries of wide significance followed, including: the recognition of the importance of pulsatile hormone secretion; the recognition of the importance of stimulus-secretion coupling mechanisms in interpreting the patterned electrical activity of neurons; the physiological importance of peptide release in the brain; the recognition that peptide release comes substantially from dendrites and can be regulated independently of nerve terminal secretion; and the importance of dynamic morphological changes to neuronal function in the hypothalamus. All of these discoveries followed from the drive to understand the milk-ejection reflex. We also reflect on Harris's observations on vasopressin secretion, on the effects of stress, and on oxytocin secretion during sexual activity.

Cortisol secretion in response to metabolic and inflammatory challenges in dairy cows.

Cortisol in dairy cows is released in an episodic manner underlying a circadian rhythm. The involvement of cortisol in numerous adaptive processes to cope with adverse conditions such as pain and inflammation is well characterized. Recent studies described contradictory effects of nutrition and metabolism on the secretory pattern of cortisol. However, up to now, the direct effects of single metabolites during various metabolic conditions without the profound endocrine changes around parturition on the glucocorticoid secretion in dairy cows have not been described. The objective of this study was to investigate the effects of long-term (56-h) manipulated metabolic states, that is, manipulated plasma concentrations of glucose and β-hydroxybutyrate (BHBA), on the release of cortisol in midlactation dairy cows. Besides the concentration of cortisol at defined time points, its pulsatile secretory pattern was studied in combination with an acute immune challenge through an intramammary lipopolysaccharide (LPS) challenge. Twenty-five midlactation dairy cows were randomly assigned to 1 of 4 treatments (hyperinsulinemic hypoglycemic clamp [HypoG], hyperinsulinemic–euglycemic clamp [EuG], continuous infusion of BHBA [HyperB], or infusion of saline solution for the control group [Control). Different metabolic states induced by infusion treatments affected the characteristics of cortisol secretion (elevation of baseline [the HypoG and HyperB treatments] and decreased peak length [the HypoG treatment]; P < 0.05), whereas amplitude, peak interval, height, peak area, area under the curve (AUC) above the baseline cortisol concentration (AUCb), and the total AUC (AUCt) were not different between infusion treatments. The induced inflammatory response due to the intramammary LPS challenge at simultaneously maintained infusion treatments diminished the pulsatile nature of cortisol release, whereas AUCb (and AUCt, respectively) was lowest for the HypoG treatment compared with the HyperB and Control treatments (P < 0.05). This study indicates that single metabolites (glucose and BHBA) and their availability or turnover (in case of glucose) have a different impact on the regulation of cortisol secretion resulting in changes of its pulsatile release. Furthermore, cortisol release during intramammary inflammation was found to be greater in the HyperB, EuG, and Control treatments compared with the HypoG treatment (P < 0.05). This finding emphasizes the regulatory role of the current metabolic status on the cortisol release during inflammation.

Detecting pulmonary capillary blood pulsations using hyperpolarized xenon-129 chemical shift saturation recovery (CSSR) MR spectroscopy.

To investigate whether chemical shift saturation recovery (CSSR) MR spectroscopy with hyperpolarized xenon-129 is sensitive to the pulsatile nature of pulmonary blood flow during the cardiac cycle. A CSSR pulse sequence typically uses radiofrequency (RF) pulses to saturate the magnetization of xenon-129 dissolved in lung tissue followed, after a variable delay time, by an RF excitation and subsequent acquisition of a free-induction decay. Thereby it is possible to monitor the uptake of xenon-129 by lung tissue and extract physiological parameters of pulmonary gas exchange. In the current studies, the delay time was instead held at a constant value, which permitted observation of xenon-129 gas uptake as a function of breath-hold time. CSSR studies were performed in 13 subjects (10 healthy, 2 chronic obstructive pulmonary disease [COPD], 1 second-hand smoke exposure), holding their breath at total lung capacity. The areas of the tissue/plasma and the red-blood-cell peaks in healthy subjects varied by an average of 1.7±0.7% and 15.1±3.8%, respectively, during the cardiac cycle. In 2 subjects with COPD these peak pulsations were not detectable during at least part of the measurement period. CSSR spectroscopy is sufficiently sensitive to detect oscillations in the xenon-129 gas-uptake rate associated with the cardiac cycle.

Mathematical modelling of time dependent flow of non-Newtonian fluid through unsymmetric stenotic tapered artery: Effects of catheter and slip velocity

In this article pulsatile nature of blood flow through unsymmetric stenosed tapered artery in the presence of catheter has been modelled. Blood is represented by micropolar fluid. The analytical solutions for velocity and microrotation components are obtained in terms of Bessel functions of the first and second kind. Flow parameters such as the resistance to flow (impedance) in the artery and wall shear stress at the maximum height of the stenosis have been calculated and the effects of various parameters such as shape parameter (\(n\)), tapered parameter (\(\zeta \)), slip velocity (\(u_{1}\), \(u_{2}\)), radius of the catheter (\(r_{c}\)), Reynolds number (\(Re\)), Strouhal number (\(\sigma \)), micropolar parameter (\(m\)), coupling number (\(N\)) and height of the stenosis (\(\epsilon \)) on impedance and wall shear stress are discussed. The locations of the maximum height of the stenosis and the annular radius which are dependent on both tapered parameter (\(\zeta \)) and shape parameter (\(n\)) are computed. It is observed that impedance is increasing while catheter radius, height of the stenosis, coupling number are increasing, while it is decreasing in case of shape parameter and micropolar parameter. Shape parameter has no effect on wall shear stress at the maximum height of the stenosis in case of non-tapered artery. However it is dependent on \(n\) in case of tapered artery. In particular wall shear stress decreases as stenosis is becoming more and more asymmetric in case of diverging tapered artery and the behaviour is exactly reverse in case of converging tapered artery. Also a comparison of the results for impedance of the present model with the experimental results of Back [4] have been carried out, it is observed that impedance increases significantly for higher values of the ratio of the radius of the catheter to that of the annular region is high.

Fluid-structure interaction in abdominal aortic aneurysms: Structural and geometrical considerations

Rupture of the abdominal aortic aneurysm (AAA) is the result of the relatively complex interaction of blood hemodynamics and material behavior of arterial walls. In the present study, the cumulative effects of physiological parameters such as the directional growth, arterial wall properties (isotropy and anisotropy), iliac bifurcation and arterial wall thickness on prediction of wall stress in fully coupled fluid-structure interaction (FSI) analysis of five idealized AAA models have been investigated. In particular, the numerical model considers the heterogeneity of arterial wall and the iliac bifurcation, which allows the study of the geometric asymmetry due to the growth of the aneurysm into different directions. Results demonstrate that the blood pulsatile nature is responsible for emerging a time-dependent recirculation zone inside the aneurysm, which directly affects the stress distribution in aneurismal wall. Therefore, aneurysm deviation from the arterial axis, especially, in the lateral direction increases the wall stress in a relatively nonlinear fashion. Among the models analyzed in this investigation, the anisotropic material model that considers the wall thickness variations, greatly affects the wall stress values, while the stress distributions are less affected as compared to the uniform wall thickness models. In this regard, it is confirmed that wall stress predictions are more influenced by the appropriate structural model than the geometrical considerations such as the level of asymmetry and its curvature, growth direction and its extent.

Simulation of Pulsatile Blood Flow Through Various Cardiac Defects and Quantitative Measurements of Shunted Blood Volume

Congenital heart defects such as Atrial Septal Defect (ASD), Ventricular Septal Defect (VSD) and Patent Ductus Arteriosus (PDA), which are the most common ones, are treated with minimally invasive surgery using occlusion devices. Newer devices have been proposed on micro- and nano-materials. To improve efficiency and to reduce failure of this mode of treatment, it is important to simulate blood flow through defect before and after placement of device and calculate shunting of blood volume. We present here blood flow through atria and aorta in normal and defect conditions. Finite Element Analysis (FEA) is used for modeling and simulation using ANSYS 14.5. Blood is simulated as Newtonian and incompressible with pulsatile nature. The model of upper two chambers of heart is modeled with and without ASD. The simulation showed shunting from left atrium to right atrium in case of ASD and volume of shunted blood is calculated with variation in shape and size of defect. PDA is modeled as tube between pulmonary artery and aorta, and shunting is calculated with variation in shape and size of PDA. The simulation can be extended further by simulating placement of device in defect and evaluating its efficiency in terms of occluding the defect. Our simulation could enable novel designs based on nano-materials and treatment modalities.

Multicellular Regulation of Tensional Homeostasis

Vascular endothelial cells are exposed to routine and directed mechanical forces due to the pulsatile nature of blood flow. As a result, these cells undergo cytoskeletal remodeling and elicit adaptive changes in cell signaling that protect them against atherosclerosis. A main purpose of this remodeling is to minimize alterations in intracellular mechanical tension caused by external forces and to maintain it at a preferred (homeostatic) level. It has been purported that normal physiological functions of the endothelium requires tensional homeostasis across a broad range of length scales, from the subcellular level to the tissue level. Our recent study challenged this view, however. We measured reorientation of cellular traction forces in isolated endothelial cells in response to periodic uniaxial stretch. We found that within ∼40-50 min from the onset of stretch the traction field reorients in the direction perpendicular to the stretch axis, but exhibits a highly dynamic and erratic behavior long after reorientation is completed. Moreover, even in the absence of external stretch the traction field remains dynamic and erratic while the cell spreading area changes very little and cells do not migrate. Here, we hypothesized that tensional homeostasis of the endothelium requires intercellular cooperation. We measured cellular traction forces in two-dimensional endothelial cell clusters of different sizes and at different length scales over an extended time period and analyzed traction dynamics. Our analysis revealed that dynamic fluctuation of traction forces diminished with increasing cluster size and with increasing strength of the traction field, suggesting that cell-cell cooperation might promote tensional homeostasis in the endothelium. Using a mathematical model, we showed that the cell clusters might regulate the homeostatic state of stress through mechanical interdependence between adjacent cells.

Cardiology patient page. Screening for critical congenital heart disease in newborns.

We have come a long way in our ability to treat critical congenital heart conditions, which affect about 3 of every 1000 live births and account for 30% of all infant fatalities in the United States annually.1 Prenatal sonograms can often identify structural heart disease; however, the sensitivity of congenital heart disease (CHD) detection is highly variable, depending on operator expertise, gestational age, fetal position, and the type of cardiac defect. As a result, prenatal sonography will miss some patients with critical CHD and is known to miss many newborns with simple CHD. Newborns who might benefit from early treatment can often be identified in their first days of life through pulse oximetry screening—a painless, readily available noninvasive examination that is easy to incorporate into newborn assessments. This noninvasive test measures the percentage of hemoglobin in the blood that is saturated with oxygen and pulse rate. The addition of pulse oximetry to fetal ultrasound and physical examination as a screening tool can reduce the chance of overlooking critical congenital heart disease (CCHD) in newborns.2 Oxygen breathed in through the lungs attaches to the red blood cell protein hemoglobin. The newly oxygenated blood then circulates to the tissues. Arterial hemoglobin saturated with oxygen is bright red, and venous hemoglobin with less oxygen is darker. Pulse oximetry uses the principles of spectrophotometry and …

Pulsatile flow of a shear-thinning model for blood through a two-dimensional stenosed channel

The effects of percentage stenosis and Reynolds number (Re) on steady flow, and Womersley number (Wo) on pulsatile flow, of blood through a two-dimensional channel with stenosis are investigated, and the results are compared with the Newtonian case. We model blood using the shear-thinning relation proposed by Yeleswarapu, while the stenosis is approximated using a cosine-shaped taper. The vorticity–streamfunction formulation of the flow equations is solved using a finite difference scheme in conjunction with a full-multigrid algorithm that reduces computational time. The presence of stenosis leads to a recirculation zone immediately downstream of the stenosis. In steady flow, the shear-thinning fluid predicts higher peak wall shear stress than the Newtonian fluid: the difference between the predictions, expressed as a percentage of the Newtonian wall shear stress, decreases as percentage stenosis and Reynolds number increase. For a given percentage stenosis and Reynolds number, the percentage difference between the shear-thinning fluid and Newtonian fluid decreases, and remains negligible, as the Womersley number increases (corresponding to increasing pulsatile nature of the flow). This suggests that the Newtonian approximation can accurately model wall shear stress in the aortic flow of blood; however, for other variables (e.g. mean velocity) the shear-thinning model is more appropriate.

Laminar shear stress regulates mitochondrial dynamics, bioenergetics responses and PRX3 activation in endothelial cells

Endothelial cells in the vascular system are constantly subjected to the frictional force of shear stress due to the pulsatile nature of blood flow. Although several proteins form part of the shear stress mechano-sensing pathway, the identification of mechano-transducing pathways is largely unknown. Given the increasing evidence for a signaling function of mitochondria in endothelial cells, the aim of this study was to investigate their role as mechano-sensor organelles during laminar shear stress (LSS). We demonstrated that LSS activates intracellular signaling pathways that modulate not only mitochondrial dynamics but also mitochondrial function. At early time points of LSS, the fission-related protein Drp1 was recruited from the cytosol to mitochondria and activated mitochondrial fission. LSS-dependent increase in intracellular Ca2+ concentration was indispensable for mitochondrial fission. As alterations in mitochondrial dynamics have been related to changes in bioenergetics profiles, we studied mitochondrial function after LSS. We found that LSS decreased respiration rate, increased mitochondrial membrane potential and promoted the mitochondrial generation of ROS with the subsequent oxidation and activation of the antioxidant enzyme PRX3. Our data support a novel and active role for mitochondria in endothelial cells as active players, able to transduce the mechanical force of shear stress in the vascular endothelium into a biological response.

Computational analysis of the effectiveness of blood flushing with saline injection from an intravascular diagnostic catheter.

Optical techniques including fluorescence lifetime spectroscopy have demonstrated potential as a tool for study and diagnosis of arterial vessel pathologies. However, their application in the intravascular diagnostic procedures has been hampered by the presence of blood hemoglobin that affects the light delivery to and the collection from the vessel wall. We report a computational fluid dynamics model that allows for the optimization of blood flushing parameters in a manner that minimizes the amount of saline needed to clear the optical field of view and reduces any adverse effects caused by the external saline jet. A 3D turbulence (k - ω) model was employed for Eulerian-Eulerian two-phase flow to simulate the flow inside and around a side-viewing fiber-optic catheter. Current analysis demonstrates the effects of various parameters including infusion and blood flow rates, vessel diameters, and pulsatile nature of blood flow on the flow structure around the catheter tip. The results from this study can be utilized in determining the optimal flushing rate for given vessel diameter, blood flow rate, and maximum wall shear stress that the vessel wall can sustain and subsequently in optimizing the design parameters of optical-based intravascular catheters.

Pulsatile blood flow in large arteries: comparative study of Burton’s and McDonald’s models

To get a clear picture of the pulsatile nature of blood flow and its role in the pathogenesis of atherosclerosis, a comparative study of blood flow in large arteries is carried out using the two widely used models, McDonald’s and Burton’s models, for the pressure gradient. For both models, the blood velocity in the lumen is obtained analytically. Elaborate investigations on the wall shear stress (WSS) and oscillatory shear index (OSI) are carried out. The results are in good agreement with the available data in the literature. The superiority of McDonald’s model in capturing the pulsatile nature of blood flow, especially the OSI, is highlighted. The present investigation supports the hypothesis that not only WSS but also OSI are the essential features determining the pathogenesis of atherosclerosis. Finally, by reviewing the limitations of the present investigation, the possibility of improvement is explored.

Molecular- and Organelle-Based Predictive Paradigm Underlying Recovery by Left Ventricular Assist Device Support

Advanced heart failure (HF) is a major cause of morbidity and mortality in the United States, and heart transplantation remains as the gold standard therapy. Because of scarcity of donor organs, the application of mechanical circulatory support devices has become a crucial approach in HF therapy as a bridge to transplantation. Therefore, mechanical circulatory support devices have existed both conceptually and experimentally for >40 years, along which an exponential evolution of mechanical circulatory support device technology has occurred. To mimic human physiology, the first generation of left ventricular assist devices (LVADs) were pulsatile volume displacement pumps (HeartMate XVE LVAS, Thoratec PVAD, and Novacor, etc). Insights demonstrating the inessentiality of the pulsatile nature of LVADs for survival from a physiological standpoint propelled the design of second-generation continuous flow devices (HeartMate II [Thoratec Inc], the Micromed DeBakey VAD, Berlin Heart Incor [Berlin Heart AG], and the Jarvik 2000 [Jarvik Heart Inc]), which emerged with superior safety and durability. Consequently, the HeartMate II was approved for bridge to transplantation and destination therapy in the United States.1 Recent reports2,3 have demonstrated a 2-year survival rate of 87% in destination therapy patients under intense surveillance, comparable with open heart transplantation survival statistics. In parallel, these promising outcomes of LVADs in HF therapy have spawned the translational research field of LV reverse remodeling, which has already shown great promise for elucidating underlying molecular and cellular mechanisms. HF is a highly complex clinical syndrome marked by a multitude of derangements, both in adult and pediatric populations.4 The clinical phenotype of HF begins with an injury or supranormal stressor on the heart and, through prolonged dyshomeostasis, eventuates in cellular and organ failure. The compensatory adaptive mechanisms including neurohormonal activation (eg, the …

Considerations of Blood Properties, Outlet Boundary Conditions and Energy Loss Approaches in Computational Fluid Dynamics Modeling

Despite recent development of computational fluid dynamics (CFD) research, analysis of computational fluid dynamics of cerebral vessels has several limitations. Although blood is a non-Newtonian fluid, velocity and pressure fields were computed under the assumptions of incompressible, laminar, steady-state flows and Newtonian fluid dynamics. The pulsatile nature of blood flow is not properly applied in inlet and outlet boundaries. Therefore, we present these technical limitations and discuss the possible solution by comparing the theoretical and computational studies.

Biological factors in plasma from diabetes mellitus patients enhance hyperglycaemia and pulsatile shear stress-induced endothelial cell apoptosis

People suffering from Diabetes Mellitus (DM) are prone to an array of vascular complications leading to end organ damage. The hallmark of these vascular complications is endothelium dysfunction, which is caused by endothelial cell (EC) apoptosis. Although the endothelial cell (EC) dysfunction induced by hyperglycaemia and fluid shear stress has been studied, the effects of biological factors in the blood of DM patients on EC integrity have not been reported in the in vitro models that mimic the physiological pulsatile nature of the vascular system. This study reports the development of a hemodynamic lab-on-a-chip system to investigate this issue. The pulsatile flow was applied to a monolayer of endothelial cells expressing a fluorescence resonance energy transfer (FRET)-based biosensor that changes colour from green to blue in response to caspase-3 activation during apoptosis. Plasma samples from healthy volunteers and DM patients were compared to identify biological factors that are critical to endothelial disruption. Three types of microchannels were designed to simulate the blood vessels under healthy and partially blocked pathological conditions. The results showed that EC apoptosis rates increased with increasing glucose concentration and levels of shear stress. The rates of apoptosis further increased by a factor of 1.4-2.3 for hyperglycaemic plasma under all dynamic conditions. Under static conditions, little difference was detected in the rate of EC apoptosis between experiments using plasma from DM patients and glucose medium, suggesting that the effects of hyperglycaemia and biological factors on the induction of EC apoptosis are all shear flow-dependent. A proteomics study was then conducted to identify biological factors, demonstrating that the levels of eight proteins, including haptoglobin and clusterin, were significantly down-regulated, while six proteins, including apolipoprotein C-III, were significantly up-regulated in the plasma of DM patients compared to healthy volunteers. This hemodynamic lab-on-a-chip system can serve as a high throughput platform to assess the risk of vascular complications of DM patients and to determine the effects of therapeutics or other interventions on EC apoptosis.

Repeating adrenal vein sampling when neither aldosterone/cortisol ratio exceeds peripheral yields a high incidence of aldosterone-producing adenoma

In primary aldosteronism, adrenal vein sampling (AVS) suggests unilateral aldosterone-producing adenoma (APA) when the aldosterone/cortisol (A/F) ratio is less than or equal to peripheral on one side and at least two times peripheral on the other. When A/F ratios are lower bilaterally than peripheral despite adequate samples (adrenal venous cortisol ≥3 times peripheral), we recommend repeat AVS. This study aimed to determine the frequency of this occurrence and outcomes in such cases. We performed a retrospective observational study of all cases of primary aldosteronism undergoing initial AVS over a 34-year period. Initial AVS in 1397 patients returned satisfactory and discriminatory results in 1066 (76.3%) but 37 patients (2.6%) had adequate samples but bilateral A/F ratios no higher than peripheral. Of the 22 of these 37 who agreed to repeat AVS, 10 demonstrated unilateral aldosterone production, and eight of these had unilateral adrenalectomy disclosing APAs and resulting in cure (3) or improvement (5) in hypertension. Eight had bilateral aldosterone production. Four studies were inconclusive. Patients with initial unsatisfactory AVS because of bilaterally low A/F ratios had significantly (P=0.023) more unilateral disease [10 of 18 satisfactory repeat studies (55.6%) vs. 326 of 1066 satisfactory initial studies (30.6%)] and a significantly higher (67.6 vs. 49.9%, P=0.034) percentage of males. As the incidence of APAs was high in a subgroup with low A/F bilaterally on initial AVS, these patients should be offered repeat AVS. This might reflect both a greater dependence of aldosterone production on adrenocorticotrophic hormone (ACTH) in APAs and the pulsatile nature of ACTH secretion.

The effect of nail polish on pulse oximetry readings

Pulse oximeters utilise the pulsatile nature of arterial blood flow to distinguish it from venous flow and estimate oxygen saturation in arterial blood. Pulse oximetry is primarily used in hospital wards, emergency rooms, intensive care units, operating rooms and home care. The objective of this study is to determine whether the use of nail polish of various colours have an effect on oximeter readings of oxygen saturation value. The sample group of this study is comprised of 40 healthy women. In the first phase of the study, readings were taken on left and right hand fingers, with no nail polish, to determine any differences in oxygen saturation value. In the second phase of the study, 10 different colours of nail polish, namely dark red, yellow, dark blue, green, purple, brown, white, metallic, black and pink, of the same brand were applied. Readings were recorded once oxygen saturation values on the screen became stable. Number and percentage distributions along with Wilcoxon signed ranks and Friedman test were used in the analysis of data. Only red nail polish did not yield statistically significant reading results. We conclude that different nail polish colours cause a clinically significant change in pulse oximeter readings in healthy volunteers.