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Introduction: ST2 is the receptor for interleukin (IL)-33, the last discovered member of the IL-1 cytokine family. Acute inflammation is an early response of vascularized tissue to injury, in which alteration of micro- and macro-elements occurs. This study aimed to examine the alteration of cobalt, sodium, potassium, and calcium concentration at the site of acute inflammation and the role of ST2 in these alterations., Material and Methods: Wild-type (WT) and ST2 knockout (ST2-/-) mice were divided into groups: WT control group (WT-C), ST2 knockout control group (KO-C), WT inflammatory group (WT-I), and ST2 knockout inflammatory group (KO-I). We induced acute inflammation by intramuscular injection of turpentine oil or saline in the case of the control group. After 12 h, we anesthetized mice and collected treated tissues for histopathological analysis and determination of cobalt, sodium, potassium, and calcium concentration by atomic absorption spectrometer., Results: Histopathological analysis showed the inflammatory infiltrate and cell necrosis in the treated tissue in WT-I and KO-I. The concentration of sodium was significantly lower in WT-I than in WT-C. The concentration of potassium and cobalt was significantly lower in WT-I and KO-I when compared to WT-C and KO-C, respectively. However, the concentration of potassium and cobalt in the tissue was significantly lower in WT-I than in KO-I. The concentration of calcium in the tissue did not significantly differ between groups., Conclusion: We reported, to our knowledge for the first time, that ST2 is involved in decreasing sodium, potassium, and cobalt concentration at the site of acute inflammation., Competing Interests: Declaration of Competing Interest None., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Aberrant sympathetic nerve activity exacerbates cardiovascular risk in hypertension and diabetes, which are common comorbidities, yet clinically sympathetic nerve activity remains poorly controlled. The hypertensive diabetic state is associated with increased reflex sensitivity and tonic drive from the peripheral chemoreceptors, the cause of which is unknown. We have previously shown hypertension to be critically dependent on the carotid body (CB) input in spontaneously hypertensive rat, a model that also exhibits a number of diabetic traits. CB overstimulation by insulin and leptin has been similarly implicated in the development of increased sympathetic nerve activity in metabolic syndrome and obesity. Thus, we hypothesized that in hypertensive diabetic state (spontaneously hypertensive rat), the CB is sensitized by altered metabolic signaling causing excessive sympathetic activity levels and dysfunctional reflex regulation., Methods: Using a hypothesis-free RNA-seq approach, we investigated potential molecular targets implicated in energy metabolism mediating CB sensitization and its regulation of sympathetic outflow in experimental hypertension. Identified targets were characterized using molecular and functional techniques assessing peripheral chemoreflex sensitivity in situ and in vivo., Results: We discovered GLP1R (glucagon-like peptide-1 receptor) expression in the CBs of rat and human and showed that its decreased expression is linked to sympathetic hyperactivity in rats with cardiometabolic disease. We demonstrate GLP1R to be localized to CB chemosensory cells, while targeted administration of GLP1R agonist to the CB lowered its basal discharge and attenuated chemoreflex-evoked blood pressure and sympathetic responses. Importantly, hyperglycemia-induced peripheral chemoreflex sensitization and associated basal sympathetic overactivity were abolished by GLP1R activation in the CB suggesting a role in a homeostatic response to high blood glucose., Conclusions: We show that GLP1 (glucagon-like peptide-1) modulates the peripheral chemoreflex acting on the CB, supporting this organ as a multimodal receptor. Our findings pinpoint CBs as potential targets for ameliorating excessive sympathetic activity using GLP1R agonists in the hypertensive-diabetic condition.

The aim of this study was to test the hypothesis that subchronic co-application of vitamins B6 and folic acid (FA) could affect heart failure (HF) induced by monocrotaline (MCT), with the modulation of oxidative stress parameters and cardiometabolic biomarkers. Biochemical and histomorphometric analyses were assessed in blank solution-exposed controls (C1 physiological saline 1 mL/kg, 1 day, n = 8; C2 physiological saline 1 mL/kg, 28 days, n = 8), MCT-induced HF ( MCT 50 mg/kg, n = 8), B6+FA (vitamin B6 7 mg·kg -1 ·day -1 , FA 5 mg·kg -1 ·day -1 ; n = 8), and MCT+B6+FA (MCT 50 mg/kg, vitamin B6 7 mg·kg -1 ·day -1 , FA 5 mg·kg -1 ·day -1 ; n = 8) in male Wistar albino rats (body mass 160 g at the start). Superoxide dismutase and glutathione peroxidase activities, thiol-, carbonyl groups, and nitrotyrosine were determined in cardiac tissue. Echocardiography was performed to confirm MCT-induced HF. The right ventricular wall hypertrophy, accompanied with significant increase of troponin T and preserved renal and liver function, has been shown in MCT-induced HF. However, these effects were not related to antioxidant effects of vitamin B6 and FA, since several parameters of oxidative stress were more pronounced after treatment. In this study, co-application of vitamins B6 and FA did not attenuate hypertrophy of the right ventricle wall but aggravated oxidative stress, which is involved in HF pathogenesis.

The paper examines the influence of acute and chronic stress on the relationship between systolic blood pressure (SBP) and pulse interval (PI) recorded from laboratory rats with different genetic predispositions for the development of the hypertensive disease. Transfer entropy (TE) was used to examine the direction of information flow between SBP and PI, spontaneous baroreflex sensitivity (BRS) was used to evaluate the ability of adaptation of PI time series to changes in SBP, and the cross-approximate entropy (XApEn) to quantify the SBP-PI synchronization. The effects of the time series length on TE estimation was also investigated in an artificial environment for the time series without a strong causal relation. The consistency of the TE estimation was achieved only for extremely long time series. The results showed that chronic stress influence on the increase in information transmission between SBP and PI (TE) while changes of (BRS) and XApEn were not noticed.

Objectives: Personalised monitoring in health applications has been recognised as part of the mobile crowdsensing concept, where subjects equipped with sensors extract information and share them for personal or common benefit. Limited transmission resources impose the use of local analyses methodology, but this approach is incompatible with analytical tools that require stationary and artefact-free data. This paper proposes a computationally efficient binarised cross-approximate entropy, referred to as (X)BinEn, for unsupervised cardiovascular signal processing in environments where energy and processor resources are limited., Methods: The proposed method is a descendant of the cross-approximate entropy ((X)ApEn). It operates on binary, differentially encoded data series split into m-sized vectors. The Hamming distance is used as a distance measure, while a search for similarities is performed on the vector sets. The procedure is tested on rats under shaker and restraint stress, and compared to the existing (X)ApEn results., Results: The number of processing operations is reduced. (X)BinEn captures entropy changes in a similar manner to (X)ApEn. The coding coarseness yields an adverse effect of reduced sensitivity, but it attenuates parameter inconsistency and binary bias. A special case of (X)BinEn is equivalent to Shannon's entropy. A binary conditional entropy for m =1 vectors is embedded into the (X)BinEn procedure., Conclusion: (X)BinEn can be applied to a single time series as an auto-entropy method, or to a pair of time series, as a cross-entropy method. Its low processing requirements makes it suitable for mobile, battery operated, self-attached sensing devices, with limited power and processor resources., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Objectives . This paper analyses temporal dependency in the time series recorded from aging rats, the healthy ones and those with early developed hypertension. The aim is to explore effects of age and hypertension on mutual sample relationship along the time axis. Methods . A copula method is applied to raw and to differentially coded signals. The latter ones were additionally binary encoded for a joint conditional entropy application. The signals were recorded from freely moving male Wistar rats and from spontaneous hypertensive rats, aged 3 months and 12 months. Results . The highest level of comonotonic behavior of pulse interval with respect to systolic blood pressure is observed at time lags τ = 0, 3, and 4, while a strong counter-monotonic behavior occurs at time lags τ = 1 and 2. Conclusion . Dynamic range of aging rats is considerably reduced in hypertensive groups. Conditional entropy of systolic blood pressure signal, compared to unconditional, shows an increased level of discrepancy, except for a time lag 1, where the equality is preserved in spite of the memory of differential coder. The antiparallel streams play an important role at single beat time lag., Competing Interests: The authors declare that there is no conflict of interests regarding the publication of this paper.

Aim: The aim of this study was to examine the role of IL-33/ST2 pathway in a pathogenesis of acute inflammation and its effects on tissue damage, antioxidative capacity, magnesium concentration and cytokine profile in acutely inflamed tissue., Material and Methods: Male mice were randomly divided in four groups: wild-type control group (WT-C), ST2 knockout control group (KO-C), wild-type inflammatory group (WT-I), and ST2 knockout inflammatory group (KO-I). Acute inflammation was induced in WT-I and KO-I by intramuscular injection of turpentine oil, while mice in WT-C and KO-C were treated with saline. After 12h, animals were euthanized, and blood was collected for determination of creatine kinase (CK) and aspartate transaminase (AST) activity. The treated tissue was used for histopathological analysis, determination of volume density of inflammatory infiltrate (Vdii) and necrotic fiber (Vdnf), gene expression of interleukin (IL)-33, ST2, tumor necrosis factor alpha (TNF-alpha), IL-6, IL-12p35, and transforming growth factor beta (TGF-beta), concentration of magnesium (Mg), copper (Cu), selenium (Se), manganese (Mn) and reduced glutathione (GSH), and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity., Results: Presence of inflammatory infiltration and necrosis in the treated tissue was histopathologically confirmed in WT-I and KO-I. Vdii was significantly higher in WT-I when compared to KO-I, whereas Vdnf did not significantly differ between WT-I and KO-I. CK and AST significantly increased in both inflammatory groups when compared to corresponding control groups. However, the values of CK and AST were significantly higher in WT-I than in KO-I. Mg in the treated tissue was significantly lower in WT-I in comparison to WT-C and KO-I, while there was no significant difference between KO-C and KO-I. There was no significant difference in Cu, Se, and Mn in the treated tissue between WT-C, KO-C, WT-I and KO-I. Gene expression of IL-33 in the treated tissue increased in both inflammatory groups when compared to the corresponding control groups, but it was significantly higher in KO-I than in WT-I. Gene expression of ST2 in the treated tissue was significantly higher in WT-I than in WT-C. Gene expression of TNF-alpha, IL-6, and IL-12p35 in the treated tissue was significantly higher in WT-I and KO-I than in the corresponding control groups, and IL-6 was significantly higher in KO-C than in WT-C. TGF-beta gene expression in the treated tissue was significantly higher in KO-I when compared to WT-I, while there was no difference between WT-C and KO-C. SOD activity decreased at the site of acute inflammation in both inflammatory groups, while the GPx activity increased. GSH in the treated tissue was significantly higher in KO-I than in KO-C or WT-I., Conclusion: The results of our study have indicated, to our knowledge for the first time, that IL-33/ST2 pathway plays a role in enhancing inflammation and tissue damage at the site of acute inflammation by affecting the concentration of magnesium and GSH, important for antioxidative capacity, as well as gene expression of anti-inflammatory cytokine TGF-beta., (Copyright © 2016 Elsevier Inc. All rights reserved.)

In this paper a copula approach is applied as a tool for assessing the measure of statistical dependence of parallel cardiovascular time series. Families of Archimedean copulas (Clayton, Frank and Gumbel) are applied to pulse interval, systolic and diastolic blood pressure recorded from male Wistar rats at baseline conditions, and to their isodistributional surrogates with the same marginal, but randomized joint distribution functions. The influence of time offset of the parallel time series is explored. The amount of data required for a stable working point is discussed.

This study proposes a method for obtaining a stable working point that enables the unbiased estimates of the approximate entropy and the sample entropy. Pattern length, normalized threshold, time delay and tines series length are levels of freedom that are considered. Pulse interval signals used for the experiment are recorded from laboratory animals with different likelihood of developing cardiovascular disease--normal and borderline hypertensive rats--exposed to the acute and to the chronic stress. It is shown that the threshold level is the major source of the instability, and that the generally accepted and widely used methods for a threshold choice may lead to an incorrect psychological interpretation. A method for the threshold level correction is proposed., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Radiotelemetred male Wistar outbrad rats and Borderline Hypertensive rats (BHR) were exposed to acute and chronic environmental stress. Approximate entropy (ApEn) approach is applied in order to investigate the pulse interval (PI) response to two different types of environmental stress: shaker and restrain stress. The performance of ApEn method was evaluated from the parameter selection point of view. The purpose of the study is to quantify the complexity of response to stress and period of recovery after the stress in order to gain an insight in consequences of chronic stress exposure.

Spectral analysis of cardiovascular series is an important tool for assessing the features of the autonomic control of the cardiovascular system. In this experiment Wistar rats ecquiped with intraarterial catheter for blood pressure (BP) recording were exposed to stress induced by blowing air. The problem of non stationary data was overcomed applying the Smoothed Pseudo Wigner Villle (SPWV) time-frequency distribution. Spectral analysis was done before stress, during stress, immediately after stress and later in recovery. The spectral indices were calculated for both systolic blood pressure (SBP) and pulse interval (PI) series. The time evolution of spectral indices showed perturbed sympathovagal balance.

This paper describes the effects of vasopressin nonpeptide selective V1a (OPC-21268) and V2 (OPC-31260) antagonists on fast blood pressure (BP) oscillations in conscious non-haemorrhaged and haemorrhaged rats. Equidistant sampling at 20 Hz allowed direct spectral analysis of BP on 30 overlapping 2048 point-time series. In non-haemorrhaged rats, V1a antagonist (5 mg/kg; i.v) reduced BP and low-frequency (LF-BP) component while subsequent administration of V2 antagonist (1 mg/kg; i.v) reversed these changes and enhanced the very low-frequency (VLF-BP) component. In haemorrhaged rats (5-15 ml/kg/min) V2 antagonist pre-treatment enhanced the VLF-BP component during normotensive bleeding, while the V1a antagonist pre-treatment modified BP variability after hypotensive haemorrhage by enhancing the HF-SBP component. The results suggest that under normotensive conditions vasopressin by the stimulation of both V1a and V2 receptors buffers BP variability in the VLF-BP frequency domain. In addition, under hypotensive conditions vasopressin, by the stimulation of V1a receptors buffers the respiration-induced HF-BP oscillation.

Spectral analysis of blood pressure fast oscillations (short-term variability), both in humans and animals, reveals three major frequential domains: the very low-, low- and the high-frequency domain. In this paper, experimental data providing evidence for physiological mechanisms involved in the regulation of blood pressure oscillations such as sympathetic nervous system, renin-angiotensin system, NO, respiration, heart function, and circulating blood volume are reviewed. In addition, novel evidence is provided by the author for vasopressin modulation of the low- and high-frequency blood pressure components. This review suggests that the multiplicity of factors involved in the genesis of the blood pressure spectral components imply utmost caution in interpreting spectral results.