Blood Pressure Volume Research Articles

Spontaneous Thoracic Spinal Epidural Hematoma During Pregnancy

Spontaneous Thoracic Spinal Epidural Hematoma During Pregnancy

Sex Modulates Cardiovascular Effects of Icodextrin-Based Peritoneal Dialysis Solutions.

Background/Aims: Some previous observations have noted that after six months of peritoneal dialysis (PD) treatment with icodextrin solutions, blood pressure (BP) and NT-proBNP tend to return to baseline values. This may be due to accumulation of icodextrin products that exert a colloid osmotic effect, which drives water into the bloodstream, causing the rise in blood pressure. Since icodextrin is metabolized by α-Amylase and its gene copies are lower in females than in males, we hypothesized icodextrin metabolites reach higher concentrations in females and that cardiovascular effects of icodextrin are influenced by sex. Methods: Secondary analysis of a RCT comparing factors influencing fluid balance control in diabetic PD patients with high or high average peritoneal transport receiving icodextrin (n = 30) or glucose (n = 29) PD solutions. Serum icodextrin metabolites, osmolality, body composition and Inferior Vena Cava (IVC) diameter were measured at baseline, and at 6 and 12 months of follow-up. Results: After six months of treatment, icodextrin metabolites showed higher levels in females than in males, particularly G5-7 and >G7, serum osmolality was lower in females. In spite of reduction in total and extracellular body water, ultrafiltration (UF) was lower and IVC diameter and BP increased in females, suggesting increment of blood volume. Conclusion: Females undergoing PD present with higher levels of icodextrin metabolites in serum that may exert an increased colloid-osmotic pressure followed by less UF volumes and increment in blood volume and blood pressure. Whether this could be due to the lesser number of α-Amylase gene copies described in diabetic females deserves further investigation.

Diet-induced hypertension in rats is associated with increased renal vasoconstrictor response to angiotensin II after imitated endothelial dysfunction.

The mechanisms behind development of diet-induced hypertension remain unclear. The kidneys play a paramount role in blood volume and blood pressure regulation. Increases in renal vascular resistance lead to increased mean arterial blood pressure (MAP) due to reduced glomerular filtration rate and Na+ excretion. Renal vascular resistance may be increased by several factors, e.g. sympathetic output, increased activity in the renin-angiotensin system or endothelial dysfunction. We examined if a 14-week diet rich in fat, fructose or both led to increased renal vascular resistance and blood pressure. Sixty male Sprague-Dawley rats received normal chow (Control), high-fat chow (High Fat), high-fructose in drinking water (High Fructose), or a combination of high-fat and high-fructose diet (High Fat + Fruc) for 14weeks from age 4-weeks. Measurements included body weight (BW), telemetry blood pressures, renal blood flow in anesthetized rats, plasma concentrations of atrial natriuretic peptide and glucose, as well as vessel myography in renal segmental arteries. Body weight increased in both groups receiving high fat, whereas MAP increased only in the High Fat + Fruc group. Renal blood flow did not differ between groups showing that renal vascular resistance was not increased by the diets. After inhibiting nitric oxide and prostacyclin production, renal blood flow reductions to Angiotensin II infusions were exaggerated in the groups receiving high fructose. MAP correlated positively with heart rate in all rats tested. Our data suggest that diet-induced hypertension is not caused by an increase in renal vascular resistance. The pathophysiological mechanisms may include altered signaling in the renin-angiotensin system and increases in central sympathetic output in combination with reduced baroreceptor sensitivity leading to increased renal vasoconstrictor responses.

Autonomic control of cerebral blood flow: fundamental comparisons between peripheral and cerebrovascular circulations in humans.

Understanding the contribution of the autonomic nervous system to cerebral blood flow (CBF) control is challenging, and interpretations are unclear. The identification of calcium channels and adrenoreceptors within cerebral vessels has led to common misconceptions that the function of these receptors and actions mirror those of the peripheral vasculature. This review outlines the fundamental differences and complex actions of cerebral autonomic activation compared with the peripheral circulation. Anatomical differences, including the closed nature of the cerebrovasculature, and differential adrenoreceptor subtypes, density, distribution and sensitivity, provide evidence that measures on peripheral sympathetic nerve activity cannot be extrapolated to the cerebrovasculature. Cerebral sympathetic nerve activity seems to act opposingly to the peripheral circulation, mediated at least in part by changes in intracranial pressure and cerebral blood volume. Additionally, heterogeneity in cerebral adrenoreceptor distribution highlights region-specific autonomic regulation of CBF. Compensatory chemo- and autoregulatory responses throughout the cerebral circulation, and interactions with parasympathetic nerve activity are unique features to the cerebral circulation. This crosstalk between sympathetic and parasympathetic reflexes acts to ensure adequate perfusion of CBF to rising and falling perfusion pressures, optimizing delivery of oxygen and nutrients to the brain, while attempting to maintain blood volume and intracranial pressure. Herein, we highlight the distinct similarities and differences between autonomic control of cerebral and peripheral blood flow, and the regional specificity of sympathetic and parasympathetic regulation within the cerebrovasculature. Future research directions are outlined with the goal to further our understanding of autonomic control of CBF in humans.

Differential influences of dietary sodium on blood pressure regulation based on race and sex.

There are clear differences between men and women, and differences among races, in the incidence and prevalence of hypertension. Furthermore, there is extensive inter-individual variability among humans in the extent to which sodium ingestion alters blood pressure. Orthostatic intolerance and orthostatic hypotension are more common in women; these are often treated with a high salt diet, which has variable efficacy in increasing blood volume and blood pressure. Conversely, people with certain forms of hypertension are often counseled to decrease their sodium intake. Non-Hispanic Black men and women have higher rates of hypertension compared to non-Hispanic White men and women and other racial/ethnic groups. In aggregate, Black women appear to have better orthostatic tolerance than White women. In the present paper, we summarize and evaluate the current evidence for mechanisms of blood pressure regulation in men and women, as well as differences between Black and White groups, with a focus on cardiovascular responses to salt and differences among these groups. We also provide a brief review of factors that are not traditionally considered to be "biological" - such as socio-economic disparities resulting from historic and contemporary inequity across racial groups. These non-biological factors have direct and substantial influences on cardiovascular mechanisms, as well as implications for the influences of salt and sodium intake on blood pressure and cardiovascular health. We conclude that both biological and socio-economic factors provide critical modulating influences when considering the impacts of sodium on cardiovascular health as functions of race and sex.

Differentiating Electrolyte and Fluid Disorders

Abstract Vasopressin or anti-diuretic hormone (ADH) is a nonapeptide that is synthesized in the hypothalamus and plays an important role in the control of the body’s osmotic balance, blood pressure regulation and kidney function. ADH induces expression of water transport proteins in the late distal tubule and collecting duct to increase water re-absorption. ADH is produced by neurons within the supraoptic nuclei of the hypothalamus, stored in secretary vesicles and transported through the hypothalamic-hypophyseal tract and released in the posterior pituitary. The secreted hormones then enter nearby fenestrated capillaries where they enter the body’s systemic circulation. These neurons express osmo receptors that are responsive to blood osmolarity and respond to changes as little as 2 mOsm/L. Therefore slight elevations in osmolarity result in secretion of ADH. ADH acts in the kidneys to increase water re-absorption, thus returning the osmolarity to baseline. ADH is also secreted in times of hypovolaemia. Decreased arterial blood volume is sensed by bar receptors in the left atrium, carotid artery and aortic arch and the signal transported to the vagus nerve which directly stimulates the release of ADH. ADH then promotes water re-absorption in the kidneys to increase effective arterial blood volume and increase blood pressure to maintain tissue perfusion. Osmolarity and volume status are the two greatest factors that affect ADH secretion. There are three pathologic states related to ADH.

Subdural hematoma in glutaric aciduria type 1: High excreters are prone to incidental SDH despite newborn screening.

Subdural hematoma (SDH) was initially reported in 20% to 30% of patients with glutaric aciduria type 1 (GA1). A recent retrospective study found SDH in 4% of patients, but not in patients identified by newborn screening (NBS). 168 MRIs of 69 patients with GA1 (age at MRI 9 days - 73.8 years, median 3.2 years) were systematically reviewed for presence of SDH, additional MR and clinical findings in order to investigate the frequency of SDH and potential risk factors. SDH was observed in eight high-excreting patients imaged between 5.8 and 24.4months, namely space-occupying SDH in two patients after minor accidental trauma and SDH as an incidental finding in six patients without trauma. In patients without trauma imaged at 3 to 30 months (n=36, 25 NBS, 27/9 high/low excreters), incidence of SDH was 16.7% (16% in NBS). SDH was more common after acute (33.3%) than insidious onset of dystonia (14.3%) or in asymptomatic patients (5.9%). It was only seen in patients with wide frontoparietal CSF spaces and frontotemporal hypoplasia. High excreters were over-represented among patients with SDH (6/27 vs 0/9 low excreters), acute onset (10/12), and wide frontoparietal CSF spaces (16/19). Incidental SDH occurs despite NBS and early treatment in approximately one in six patients with GA1 imaged during late infancy and early childhood. Greater risk of high excreters is morphologically associated with more frequent enlargement of external CSF spaces including frontotemporal hypoplasia, and may be furthered aggravated by more pronounced alterations of cerebral blood volume and venous pressure.

Credibility Assessment of a Subject-Specific Mathematical Model of Blood Volume Kinetics for Prediction of Physiological Response to Hemorrhagic Shock and Fluid Resuscitation.

Subject-specific mathematical models for prediction of physiological parameters such as blood volume, cardiac output, and blood pressure in response to hemorrhage have been developed. In silico studies using these models may provide an effective tool to generate pre-clinical safety evidence for medical devices and help reduce the size and scope of animal studies that are performed prior to initiation of human trials. To achieve such a goal, the credibility of the mathematical model must be established for the purpose of pre-clinical in silico testing. In this work, the credibility of a subject-specific mathematical model of blood volume kinetics intended to predict blood volume response to hemorrhage and fluid resuscitation during fluid therapy was evaluated. A workflow was used in which: (i) the foundational properties of the mathematical model such as structural identifiability were evaluated; (ii) practical identifiability was evaluated both pre- and post-calibration, with the pre-calibration results used to determine an optimal splitting of experimental data into calibration and validation datasets; (iii) uncertainty in model parameters and the experimental uncertainty were quantified for each subject; and (iv) the uncertainty was propagated through the blood volume kinetics model and its predictive capability was evaluated via validation tests. The mathematical model was found to be structurally identifiable. Pre-calibration identifiability analysis led to splitting the 180 min of time series data per subject into 50 and 130 min calibration and validation windows, respectively. The average root mean squared error of the mathematical model was 12.6% using the calibration window of (0 min, 50 min). Practical identifiability was established post-calibration after fixing one of the parameters to a nominal value. In the validation tests, 82 and 75% of the subject-specific mathematical models were able to correctly predict blood volume response when predictive capability was evaluated at 180 min and at the time when amount of infused fluid equals fluid loss.

Norepinephrine potentiates the efficacy of volume expansion on mean systemic pressure in septic shock

BackgroundThrough venous contraction, norepinephrine (NE) increases stressed blood volume and mean systemic pressure (Pms) and exerts a “fluid-like” effect. When both fluid and NE are administered, Pms may not only result from the sum of the effects of both drugs. Indeed, norepinephrine may enhance the effects of volume expansion: because fluid dilutes into a more constricted, smaller, venous network, fluid may increase Pms to a larger extent at a higher than at a lower dose of NE. We tested this hypothesis, by mimicking the effects of fluid by passive leg raising (PLR).MethodsIn 30 septic shock patients, norepinephrine was decreased to reach a predefined target of mean arterial pressure (65–70 mmHg by default, 80–85 mmHg in previously hypertensive patients). We measured the PLR-induced increase in Pms (heart–lung interactions method) under high and low doses of norepinephrine. Preload responsiveness was defined by a PLR-induced increase in cardiac index ≥ 10%.ResultsNorepinephrine was decreased from 0.32 [0.18–0.62] to 0.26 [0.13–0.50] µg/kg/min (p < 0.0001). This significantly decreased the mean arterial pressure by 10 [7–20]% and Pms by 9 [4–19]%. The increase in Pms (∆Pms) induced by PLR was 13 [9–19]% at the higher dose of norepinephrine and 11 [6–16]% at the lower dose (p < 0.0001). Pms reached during PLR at the high dose of NE was higher than expected by the sum of Pms at baseline at low dose, ∆Pms induced by changing the norepinephrine dose and ∆Pms induced by PLR at low dose of NE (35.6 [11.2] mmHg vs. 33.6 [10.9] mmHg, respectively, p < 0.01). The number of preload responders was 8 (27%) at the high dose of NE and 15 (50%) at the low dose.ConclusionsNorepinephrine enhances the Pms increase induced by PLR. These results suggest that a bolus of fluid of the same volume has a greater haemodynamic effect at a high dose than at a low dose of norepinephrine during septic shock.

Expert consensus on the use of human serum albumin in critically ill patients.

Expert consensus on the use of human serum albumin in critically ill patients.

Fludrocortisone for orthostatic hypotension.

Orthostatic hypotension is an excessive fall in blood pressure (BP) while standing and is the result of a decrease in cardiac output or defective or inadequate vasoconstrictor mechanisms. Fludrocortisone is a mineralocorticoid that increases blood volume and blood pressure. Fludrocortisone is considered the first- or second-line pharmacological therapy for orthostatic hypotension alongside mechanical and positional measures such as increasing fluid and salt intake and venous compression methods. However, there has been no Cochrane Review of the benefits and harms of this drug for this condition. To identify and evaluate the benefits and harms of fludrocortisone for orthostatic hypotension. We searched the following databases on 11 November 2019: Cochrane Neuromuscular Specialised Register, CENTRAL, MEDLINE, Embase and CINAHL. We also searched trials registries. We included all studies evaluating the benefits and harms of fludrocortisone compared to placebo, another drug for orthostatic hypotension, or studies without comparators, including randomized controlled trials (RCTs), quasi-RCTs and observational studies. We included studies in people with orthostatic hypotension due to a chronic peripheral neuropathy, a central autonomic neuropathy, or autonomic failure from other causes, but not medication-induced orthostatic hypotension or orthostatic hypotension from acute volume depletion or blood loss. We usedCochrane methodological procedures for most of the review. We developed and used a tool to prioritize observational studies that offered the best available evidence where there are gaps in the evidencefrom RCTs. We assessed the certainty of evidence for fludrocortisone versus placebo using GRADE. We included 13 studies of 513 participants, including three cross-over RCTs and 10 observational studies (three cohort studies, six case series and one case-control study). The included RCTs were small (total of 28 participants in RCTs), short term (two to three weeks), only examined fludrocortisone for orthostatic hypotension in people with two conditions (diabetes and Parkinson disease), and had variable risk of bias (two had unclear risk of bias and one had low risk of bias). Heterogeneity in participant populations, comparators and outcome assessment methods prevented meta-analyses of the RCTs. We found very low-certainty evidence about the effects of fludrocortisone versus placebo on drop in BP in people with diabetes (-26 mmHg versus -39 mmHg systolic; -7 mmHg versus -11 mmHg diastolic; 1 cross-over study, 6 participants). For people with Parkinson disease, we found very-low certainty evidence about the effects of fludrocortisone on drop in BP compared to pyridostigmine (-14 mmHg versus -22.1 mmHg diastolic; P = 0.036; 1 cross-over study, 9 participants) and domperidone (no change after treatment in either group;1 cross-over study, 13 participants). For orthostatic symptoms, we found very low-certainty evidence for fludrocortisone versus placebo in people with diabetes (4 out of 5 analyzed participants had improvements in orthostatic symptoms, 1 cross-over study, 6 participants), for fludrocortisone versus pyridostigmine in people with Parkinson disease (orthostatic symptoms unchanged;1 cross-over study, 9 participants) or fludrocortisone versus domperidone (improvement to 6 for both interventions on the Composite Autonomic Symptom Scale-Orthostatic Domain (COMPASS-OD);1 cross-over study, 13 participants). Evidence on adverse events was also very low-certainty in both populations, but indicated side effects were minimal. Observational studies filled some gaps in evidence by examining the effects in larger groups of participants, with more diverse conditions, over longer periods of time. One cohort study (341 people studied retrospectively) found fludrocortisone may not be harmful in the long term for familial dysautonomia. However, it is unclear if this translates to long-term improvements in BP drop or a meaningful improvement in orthostatic symptoms. The evidence is very uncertain about the effects of fludrocortisone on blood pressure, orthostatic symptoms or adverse events in people with orthostatic hypotension and diabetes or Parkinson disease. There is a lack of information on long-term treatment and treatment of orthostatic hypotension in other disease states. There is a need for standardized reporting of outcomes and for standardization of measurements of blood pressure in orthostatic hypotension.

Hypertension due to loss of water

In the current issue of Acta Physiologica, two papers are published investigating the development of arterial hypertension under conditions of pathological loss of free water in two disease models. Kovaric et al 1 studied rats with chronic renal failure, shedding excessive free water via their remnant kidney due to a hypostenuric concentrating defect. Wild et al. 2 investigated a transgenic mouse model for psoriasis, losing free water via the psoriatic skin lesions. In both cases the animals displayed hypertension, cutaneous vasoconstriction, and metabolic adaptations towards enhanced production of urea and organic osmolytes typical for a phylogenetically ancient water conservation response termed aestivation 3 . The international consortia of investigators spearheaded by Titze, Karbach, and Kitada therefore conclude that in both cases the hypertension was due to cutaneous vasoconstriction in an attempt to limit epidermal water loss. Because in either case the hypertension was associated with loss of water, and thus with hypo- rather than hypervolemia, the authors argue, that this concept of pathogenesis of hypertension is antipodal to the classic view that relies on hypervolemia due to sodium retention.

Effects of positive end-expiratory pressure, carbon dioxide and body position on intracranial pressure measured by ultrasound assessment of optic nerve sheath diameter

Introduction. The optic nerve is surrounded by layers of meninges and cerebrospinal fluid, which is why intracranial pressure affects the optic nerve sheath. Noninvasive measurement of the optic nerve sheath diameter is simple, accurate, repeatable and with minimal side effects. Effects of positive end-expiratory pressure on intracranial pressure. The application of positive end-expiratory pressure plays a significant role in improving gas exchange, but it leads to an increase in intrathoracic and central venous pressure, cerebral blood volume, reduces arterial and cerebral perfusion pressure and thus futher increases intracranial pressure. The effect of positive end-expiratory pressure depends on basal intracranial pressure and respiratory system compliance. Effects of carbon dioxide on intracranial pressure. Hypercapnia leads to cerebral vasodilatation and increases cerebral blood flow and intracranial pressure. Hypocapnia reduces intracranial pressure, but its prolonged effect may lead to cerebral ischemia. Effects of body position on intracranial pressure. Body position affects intracranial pressure, primarily by affecting cerebral venous drainage. Conclusion. Body position, application of positive end-expiratory pressure, and changes in carbon dioxide can affect intracranial pressure, which is why its monitoring is of importance. Numerous studies show that their effects on intracranial pressure can be easily monitored by ultrasound assessment of optic nerve sheath diameter.

An Angiotensin-Responsive Connection from the Lamina Terminalis to the Paraventricular Nucleus of the Hypothalamus Evokes Vasopressin Secretion to Increase Blood Pressure in Mice.

Blood pressure is controlled by endocrine, autonomic, and behavioral responses that maintain blood volume and perfusion pressure at levels optimal for survival. Although it is clear that central angiotensin type 1a receptors (AT1aR; encoded by the Agtr1a gene) influence these processes, the neuronal circuits mediating these effects are incompletely understood. The present studies characterize the structure and function of AT1aR neurons in the lamina terminalis (containing the median preoptic nucleus and organum vasculosum of the lamina terminalis), thereby evaluating their roles in blood pressure control. Using male Agtr1a-Cre mice, neuroanatomical studies reveal that AT1aR neurons in the area are largely glutamatergic and send projections to the paraventricular nucleus of the hypothalamus (PVN) that appear to synapse onto vasopressin-synthesizing neurons. To evaluate the functionality of these lamina terminalis AT1aR neurons, we virally delivered light-sensitive opsins and then optogenetically excited or inhibited the neurons while evaluating cardiovascular parameters or fluid intake. Optogenetic excitation robustly elevated blood pressure, water intake, and sodium intake, while optogenetic inhibition produced the opposite effects. Intriguingly, optogenetic excitation of these AT1aR neurons of the lamina terminalis also resulted in Fos induction in vasopressin neurons within the PVN and supraoptic nucleus. Further, within the PVN, selective optogenetic stimulation of afferents that arise from these lamina terminalis AT1aR neurons induced glutamate release onto magnocellular neurons and was sufficient to increase blood pressure. These cardiovascular effects were attenuated by systemic pretreatment with a vasopressin-1a-receptor antagonist. Collectively, these data indicate that excitation of lamina terminalis AT1aR neurons induces neuroendocrine and behavioral responses that increase blood pressure.SIGNIFICANCE STATEMENT Hypertension is a widespread health problem and risk factor for cardiovascular disease. Although treatments exist, a substantial percentage of patients suffer from "drug-resistant" hypertension, a condition associated with increased activation of brain angiotensin receptors, enhanced sympathetic nervous system activity, and elevated vasopressin levels. The present study highlights a role for angiotensin Type 1a receptor expressing neurons located within the lamina terminalis in regulating endocrine and behavioral responses that are involved in maintaining cardiovascular homeostasis. More specifically, data presented here reveal functional excitatory connections between angiotensin-sensitive neurons in the lamina terminals and vasopressin neurons in the paraventricular nucleus of the hypothalamus, and further indicate that activation of this circuit raises blood pressure. These neurons may be a promising target for antihypertensive therapeutics.

Sodium Intake and Heart Failure.

Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium homeostasis and myocardial contractility. Excessive sodium intake is associated with the development of a variety of comorbidities including hypertension, chronic kidney disease, stroke, and cardiovascular diseases. While the American College of Cardiology/American Heart Association/Heart Failure Society of America guidelines recommend limiting sodium intake to both prevent and manage heart failure, the evidence behind such recommendations is unclear. Our review article highlights evidence and underlying mechanisms favoring and contradicting limiting sodium intake in heart failure.

Transcapillary transport of water, small solutes and proteins during hemodialysis

The semipermeable capillary walls not only enable the removal of excess body water and solutes during hemodialysis (HD) but also provide an essential mechanism for maintaining cardiovascular homeostasis. Here, we investigated transcapillary transport processes on the whole-body level using the three-pore model of the capillary endothelium with large, small and ultrasmall pores. The transcapillary transport and cardiovascular response to a 4-h hemodialysis (HD) with 2 L ultrafiltration were analyzed by simulations in a virtual patient using the three-pore model of the capillary wall integrated in the whole-body compartmental model of the cardiovascular system with baroreflex mechanisms. The three-pore model revealed substantial changes during HD in the magnitude and direction of transcapillary water flows through small and ultrasmall pores and associated changes in the transcapillary convective transport of proteins and small solutes. The fraction of total capillary hydraulic conductivity attributed to ultrasmall pores was found to play an important role in the transcapillary water transport during HD thus influencing the cardiovascular response to HD. The presented model provides a novel computational framework for a detailed analysis of microvascular exchange during HD and as such may contribute to a better understanding of dialysis-induced changes in blood volume and blood pressure.

Application value of serum sST2 in diagnosis and prognosis of heart failure

The incidence of heart failure (HF) increases significantly as people age. HF remains a major concern in public health. Although remarkable achievements have been made to treat heart failure in recent years, the survival rate of patients is still very low and the prognosis is poor. The mortality rate within 5 years after the diagnosis of heart failure is up to 50%. If we can quickly and effectively diagnose heart failure and reasonably stratify according to the risk, it will provide a solid foundation for clinicians to formulate treatment plans. Biomarkers play an important role in the diagnosis, curative effect evaluation and prognosis of heart failure. Heart failure is a complex disease in which various pathophysiological processes are involved over time. When heart failure occurs, neuroendocrine system is activated. With the increase of blood volume and ventricular wall pressure, ventricular myocytes secrete NT-proBNP/BNP. Therefore, NT-proBNP/BNP can be used as a biomarker for diagnosis and prognosis of heart failure. However, NT-proBNP/BNP in plasma is easily affected by many factors such as age, sex, body type, left ventricular hypertrophy, tachycardia, right ventricular overload, hypoxemia, and kidney function. As a novel marker of heart failure, sST2 has attracted much attention in recent years. It can reflect the degree of myocardial fibrosis and predict whether ventricular remodeling will occur. It is worth noting that sST2 is not affected by age, gender and renal function and other factors. Also, with low reference change values and individuality index values, sST2 seems to be the best candidate for monitoring and guided therapy. In short, sST2 is one of the ideal indicators to evaluate heart failure. This review summarizes the research progress of sST2 in the diagnosis and prognosis of heart failure in recent years, and provides perspectives for its future development.

Mechanism of Qingfei Paidu decoction for treatment of COVID-19: analysis based on network pharmacology and molecular docking technology

To explore the target, signaling pathways and their biological functions of Qingfei Paidu Decoction in the treatment of COVID-19 based on network pharmacology and molecular docking technology. The active components and target proteins in 21 drugs such as Ephedrae Herba and Pinelliae Rhizoma in Qingfei Paidu decoction were analyzed, and the signaling pathways and biological functions of the target proteins common with COVID-19 were screened by using TCMSP, Swiss Target Prediction, CooLGeN, GeneCards, DAVID and other databases. The network diagram of Qingfei Paidu decoction was constructed using Gephi software. We identified 163 active ingredients, including MOL004798, MOL000519, MOL004824, MOL000554, MOL010428, and MOL013443, from 18 drugs in Qingfei Paidu decoction (such as Ephedrae Herba, Pinelliae Rhizoma, Glycyrrhizae Radix Et Rhiizoma, Farfarae Flos, Asteris Radix Et Rhizoma and Aurantii Fructus Immaturus). These ingredients activate renin-angiotensin system signaling pathway and apoptosis signaling pathway by regulating 10 protein targets (ACE, ACE2, AGTR1, FURIN, TNF, CASP3, CASP6, DPP4, MCL1 and POLD1) to execute 42 biological functions such as renin-angiotensin regulation of blood volume and systemic arterial blood pressure to treat COVID-19. The results of preliminary molecular docking showed that MOL000519 (from Pinelliae Rhizoma), MOL000554 (from Farfarae Flos), MOL004798 (from Ephedrae Herba), MOL004824 (from Glycyrrhizae Radix Et Rhiizoma), MOL010428 (from Asteris Radix Et Rhizoma), and MOL013443 (from Aurantii Fructus Immaturus) had good affinity with SARS-CoV-2 3CL hydrolase to form complexes with stable conformations and high binding activity (binding energy ≤- 5 kJ/mol). Qingfei Paidu decoction can treat COVID-19 through its multiple medicinal ingredients that have multiple targets and involve multiple signaling pathways for different biological functions. Our finding provides reference for further investigation into the pharmacological mechanism of Qingfei Paidu decoction in treating COVID-19.

The supine position improves but does not normalize the blunted pulmonary capillary blood volume response to exercise in mild COPD.

Patients with mild chronic obstructive pulmonary disease (COPD) demonstrate resting pulmonary vascular dysfunction as well as a blunted pulmonary diffusing capacity (DLCO) and pulmonary capillary blood volume (VC) response to exercise. The transition from the upright to supine position increases central blood volume and perfusion pressure, which may overcome microvascular dysfunction in an otherwise intact alveolar-capillary interface. The present study examined whether the supine position normalized DLCO and VC responses to exercise in mild COPD. Sixteen mild COPD participants and 13 age-, gender-, and height-matched controls completed DLCO maneuvers at rest and during exercise in the upright and supine position. The multiple -DLCO method was used to determine DLCO, VC, and membrane diffusion capacity (DM). All three variables were adjusted for alveolar volume (DLCOAdj, VCAdj, and DMAdj). The supine position reduced alveolar volume similarly in both groups, but oxygen consumption and cardiac output were unaffected. DLCOAdj, DMAdj, and VCAdj were all lower in COPD. These same variables all increased with upright and supine exercise in both groups. DLCOAdj was unaffected by the supine position. VCAdj increased in the supine position similarly in both groups. DMAdj was reduced in the supine position in both groups. While the supine position increased exercise VCAdj in COPD, the increase was of similar magnitude to healthy controls; therefore, exercise VC remained blunted in COPD. The persistent reduction in exercise DLCO and VC when supine suggests that pulmonary vascular destruction is a contributing factor to the blunted DLCO and VC response to exercise in mild COPD.NEW & NOTEWORTHY Patients with mild chronic obstructive pulmonary disease demonstrate a combination of reversible pulmonary microvascular dysfunction and irreversible pulmonary microvascular destruction.

Real-Time Multi-Modal Estimation of Dynamically Evoked Emotions Using EEG, Heart Rate and Galvanic Skin Response.

Emotion estimation systems based on brain and physiological signals such as electro encephalography (EEG), blood-volume pressure (BVP), and galvanic skin response (GSR) are gaining special attention in recent years due to the possibilities they offer. The field of human-robot interactions (HRIs) could benefit from a broadened understanding of the brain and physiological emotion encoding, together with the use of lightweight software and cheap wearable devices, and thus improve the capabilities of robots to fully engage with the users emotional reactions. In this paper, a previously developed methodology for real-time emotion estimation aimed for its use in the field of HRI is tested under realistic circumstances using a self-generated database created using dynamically evoked emotions. Other state-of-the-art, real-time approaches address emotion estimation using constant stimuli to facilitate the analysis of the evoked responses, remaining far from real scenarios since emotions are dynamically evoked. The proposed approach studies the feasibility of the emotion estimation methodology previously developed, under an experimentation paradigm that imitates a more realistic scenario involving dynamically evoked emotions by using a dramatic film as the experimental paradigm. The emotion estimation methodology has proved to perform on real-time constraints while maintaining high accuracy on emotion estimation when using the self-produced dynamically evoked emotions multi-signal database.