1,781 research outputs found

    Air quality self-management in asthmatic patients with COPD: An integrative review for developing nursing interventions to prevent exacerbations

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    Objectives: Asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) patients experience a lower quality of life, frequent exacerbations, and worse pulmonary function. Environmental management is essential in a complex chronic condition, as pollutant exposure can worsen symptoms and increase morbidity and mortality. We aimed to identify evidence that informs nursing interventions in promoting self-management of air quality in asthmatic people with COPD. Methods: We conducted an integrative review in March of 2023. We searched the databases CINAHL, MEDLINE, Academic Search Complete, Cochrane Database of Systematic Reviews (CDSR), Scopus, Web of Science, Joanna Briggs Institute (JBI) Evidence-Based Practice Database, and Google Scholar. We included articles whose participants were adults with asthma, COPD, or both; the intervention was air quality management and the outcome of any exacerbations. We excluded editorials, letters, commentaries, opinion papers, position papers, study protocols, conference abstracts, and reviews. Data extraction and synthesis were performed, categorizing interventions according to nursing actions. Methodological quality assessment was conducted using the JBI Critical Appraisal Checklist tools. The review protocol was registered at Open Science Framework (https://doi.org/10.17605/OSF.IO/5Y4KW). Results: We included five articles from different countries. The interventions promoting air quality self-management for individuals with asthma and COPD included vigilance interventions (health professional regular visits, assessment of symptoms), monitoring interventions (measurement of indoor and outdoor trigger factors), and educational interventions (air quality alerts, allergen avoidance). Policy interventions such as smoke-free policies and comprehensive strategies to improve air quality were also identified. These areas of focus represent critical components of nurses' interventions and can integrate the fundamental patterns of knowing in nursing. Although the studies reveal heterogeneous interventions and the methodological quality is variable, these interventions showed potential for preventing exacerbations, reducing emergency department visits, and minimizing hospitalizations. Conclusions: The study emphasizes the need for a comprehensive approach involving nurses in multidisciplinary teams to air quality self-management. They can use these results to inform their interventions and ways of knowing, benefiting individuals with asthma and COPD. Further research is needed to expand the evidence base and refine these interventions.info:eu-repo/semantics/publishedVersio

    Differential right and left ventricular diastolic tolerance to acute afterload and NCX gene expression in Wistar rats

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    This study evaluated right ventricular (RV) and left ventricular (LV) diastolic tolerance to afterload and SERCA2a, phospholamban and sodium-calcium exchanger (NCX) gene expression in Wistar rats. Time constant tau and end-diastolic pressure-dimension relation (EDPDR) were analyzed in response to progressive RV or LV afterload elevations, induced by beat-to-beat pulmonary trunk or aortic root constrictions, respectively. Afterload elevations decreased LV-tau, but increased RV-tau. Whereas LV-tau analyzed the major course of pressure fall, RV-tau only assessed the last fourth. Furthermore, RV afterload elevations progressively upward shifted RV-EDPDR, whilst LV afterload elevations did not change LV-EDPDR. SERCA2a and phospholamban mRNA were similar in both ventricles. NCX-mRNA was almost 50% lower in RV than in LV. Left ventricular afterload elevations, therefore, accelerated the pressure fall and did not induce diastolic dysfunction, indicating high LV diastolic tolerance to afterload. On the contrary, RV afterload elevations decelerated the late RV pressure fall and induced diastolic dysfunction, indicating small RV diastolic tolerance to afterload. These results support previous findings relating NCX with late Ca2+ reuptake, late relaxation and diastolic dysfunction

    Differential right and left ventricular diastolic tolerance to acute afterload and NCX gene expression in Wistar rats

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    This study evaluated right ventricular (RV) and left ventricular (LV) diastolic tolerance to afterload and SERCA2a, phospholamban and sodium-calcium exchanger (NCX) gene expression in Wistar rats. Time constant tau and end-diastolic pressure-dimension relation (EDPDR) were analyzed in response to progressive RV or LV afterload elevations, induced by beat-to-beat pulmonary trunk or aortic root constrictions, respectively. Afterload elevations decreased LV-tau, but increased RV-tau. Whereas LV-tau analyzed the major course of pressure fall, RV-tau only assessed the last fourth. Furthermore, RV afterload elevations progressively upward shifted RV-EDPDR, whilst LV afterload elevations did not change LV-EDPDR. SERCA2a and phospholamban mRNA were similar in both ventricles. NCX-mRNA was almost 50% lower in RV than in LV. Left ventricular afterload elevations, therefore, accelerated the pressure fall and did not induce diastolic dysfunction, indicating high LV diastolic tolerance to afterload. On the contrary, RV afterload elevations decelerated the late RV pressure fall and induced diastolic dysfunction, indicating small RV diastolic tolerance to afterload. These results support previous findings relating NCX with late Ca2+ reuptake, late relaxation and diastolic dysfunction

    Ventricular BNP gene expression in acute cardiac overload

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    INTRODUCTION:B-type natriuretic peptide (BNP) plasma levels have important diagnostic and prognostic implications in heart failure (HF). Recently, aside from its natriuretic effect, antiproliferative and antifibrotic actions of BNP on the cardiovascular system have been described. Under physiological conditions the atria are the main source of this peptide, while its ventricular expression is still controversial. The aim of this work was to evaluate, in an animal model, the ventricular expression of BNP in normal hearts, at baseline and under acute cardiac overload.METHODS:Anesthetized open chest male Wistar rats (n=18) were instrumented with a micromanometer in the right ventricular cavity for pressure assessment. Randomization for three different protocols was then performed: (i) pressure overload for a period of 6 hours (SPr; n = 6), by pulmonary trunk banding, in order to double basal right ventricular systolic pressure; (ii) volume overload with a six-hour perfusion of Dextran 40 (SVol; n = 6), to raise end-diastolic right ventricular pressure fourfold; (iii) sham operated rats (n = 6). Transmural samples from the right ventricular free wall were then obtained for quantification of BNP mRNA by RT and quantitative real-time PCR. The results are expressed as mean+/-SEM (number molecules of mRNA BNP)/(ng total mRNA); p < 0.05.RESULTS:A basal expression of BNP was identified in the sham group (3.6x10(7) +/- 1.7x10(7)). BNP mRNA levels were elevated in both the SPr and SVol groups (+123.1 +/- 46.3% SPr and +171.6 +/- 87.7% SVol).CONCLUSIONS:Acute cardiac pressure and volume overload are associated with increased ventricular BNP gene expression. Our results suggest that BNP may be involved in early ventricular remodeling

    LLC tumor cells-derivated factors reduces adipogenesis in co-culture system

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    Cancer cachexia (CC) is a multifactorial syndrome with an unknown etiology. The primary symptom is the progressive reduction of the body weight. Recently, down-regulation of adipogenic and lipogenic genes were demonstrated to be early affected during cachexia progression in adipose tissue (AT), resulting in AT remodeling. Thus, this study aimed to evaluate in a co-culture system the influence of the Lewis Lung Carcinoma (LLC) tumor cells (c/c-LLC) in an established pre-adipocyte cell line 3T3-L1 adipogenic capacity. c/c-LLC in the presence of 3T3-L1 caused a reduction in lipids accumulation, suggesting that secretory tumor cells products may affect adipogenesis. Interestingly, a very early (day 2) down-regulation of proliferator-activated receptor gamma (PPARgamma) and CCAAT/enhancer-binding protein alpha (C/EBPalpha), followed by late genes (day 4 and 8), adiponectin, perilipin, and fatty acid-binding protein 4 (FABP4). Caspase-3 expression was increased on the last day of cell differentiation; it occurred in the expression of pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha). Overall, our results suggest that LLC secretory products impair adipocyte differentiation in a co-culture system and increased apoptosis. In summary, our study has shown the inhibition of the adipogenic process in the 3T3-L1 co-culture system with LLC cells

    Contractile effects of Ghrelin and expression of its receptor GHS-R1a in normal and hypertrophic myocardium

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    INTRODUCTION:Ghrelin, isolated in 1999, is an endogenous ligand for the growth hormone secretagogue receptor (GHS-R1a). Recent studies suggest that it may influence the function of normal and failing hearts. Nonetheless, it has been difficult to differentiate its effects on the intrinsic properties of the myocardium from the secondary effects resulting from growth hormone release and vasomotor action. This study investigated the contractile effects of ghrelin and expression of its receptor GHS-R1a in normal and hypertrophic myocardium.METHODS:Adult Wistar rats randomly received monocrotaline (MCT; n=9; 60 mg/kg, s.c.) or vehicle (n=7; 1 ml/kg). Three weeks later, after right ventricular (RV) hemodynamic evaluation, the effects of 10(-6) M of a pentapeptide active fragment of ghrelin (fG) were tested on contractile parameters of RV papillary muscles (Normal, n=7; MCT, n=9). GHS-R1a mRNA expression was estimated in RV transmural free-wall samples (Normal, n=7; MCT, n=9), using real-time RT-PCR.RESULTS:In the Normal group, fG reduced active tension (AT), maximum velocity of tension rise (dT/dt(max)) and maximum velocity of tension decline (dT/dt(min)), by 27.9 +/- 4.0%, 28.5 +/- 6.7% and 21.4 +/- 4.2% respectively. In the MCT group, fG reduced AT, dT/dt(max) and dT/dt(min) by 24.1 +/- 6.3%, 24.3 +/- 6.5% and 24.5 +/- 6.1% respectively. GHS-R1a mRNA expression was similar in the two groups (Normal: 2.3*10(5) +/- 5.4*10(4); MCT: 3.0*10(5) +/- 1.1*10(5): p > 0.05).CONCLUSION:This study shows that ghrelin has negative inotropic and lusitropic effects. These effects and expression of its receptor are preserved in RV hypertrophy, suggesting that ghrelin may be a new target in progression to heart failure

    Apelin decreases myocardial injury and improves right ventricular function in monocrotaline-induced pulmonary hypertension

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    Falcao-Pires I, Goncalves N, Henriques-Coelho T, Moreira-Goncalves D, Roncon-Albuquerque R Jr, Leite-Moreira AF. Apelin decreases myocardial injury and improves right ventricular function in monocrotaline-induced pulmonary hypertension. Am J Physiol Heart Circ Physiol 296: H2007-H2014, 2009. First published April 3, 2009; doi: 10.1152/ajpheart.00089.2009.-We investigated the endogenous production of apelin and the cardiac and pulmonary effects of its chronic administration in monocrotaline (MCT)-induced pulmonary hypertension (PH). Male Wistar rats were injected with MCT (60 mg/kg sc) or vehicle (day 0). One week later, these animals were randomly treated during 17 days with pyroglutamylated apelin-13 (Pyr-AP13; 200 mu g.kg(-1).day(-1) ip) or a similar volume of saline, resulting in four groups: sham (n = 11), sham-AP (n = 11), MCT (n = 16), and MCT-AP (n = 13). On day 25, right ventricular (RV) and left ventricular (LV) hemodynamic and morphometric parameters were assessed. Tissue and plasma samples were collected for histological and molecular analysis. When compared with sham, the MCT group presented a significant increase of RV mass (166 +/- 38%), diameter of cardiomyocyte (40 +/- 10%), myocardial fibrosis (95 +/- 20%), peak systolic pressure (99 +/- 22%), peak rate of ventricular pressure rise (dP/dt(max); 74 +/- 24%), peak rate of ventricular pressure decline (dP/dt(min); 73 +/- 19%), and time constant tau (55 +/- 16%). In these animals, RV expression of apelin (-73 +/- 10%) and its receptor APJ (-61 +/- 20%) was downregulated, whereas mRNA expression of type B natriuretic peptide (9,606 +/- 713%), angiotensinogen (191 +/- 147%), endothelin-1 (RV, 497 +/- 156%; and LV, 799 +/- 309%), plasmatic levels of apelin (104 +/- 48%), and angiotensin 1-7 (161 +/- 151%) were increased. Chronic treatment with Pyr-AP13 significantly attenuated or normalized these changes, preventing apelin-APJ mRNA downregulation and PH-induced neurohumoral activation of several vasoconstrictors, which exacerbates apelin-APJ vasodilator effects. Therefore, apelin delayed the progression of RV hypertrophy and diastolic dysfunction. Together, these observations suggest that the apelin-APJ system may play an important role in the pathophysiology of PH, representing a potential therapeutic target since it significantly attenuates RV overload and PH-induced neurohumoral activation

    Activation profile of pro-inflammatory cytokines in acute cardiac overload

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    INTRODUCTION:Pro-inflammatory cytokines have been implicated in ventricular remodeling during heart failure progression. In the present study, we investigated the effects of acute volume and RV pressure overload on biventricular hemodynamics and myocardial gene expression of IL-6 and TNF-alpha.METHODS:Male Wistar rats (n = 45) instrumented with RV and LV tip micromanometers were randomly assigned to one of three protocols: i) acute RV pressure overload (PrOv) induced by pulmonary trunk banding in order to double RV peak systolic pressure, for 120 or 360 min; ii) acute volume overload (VolOv) induced by dextran40 infusion (5 ml/h), for 120 or 360 min; iii) Sham. Free wall samples from the RV and LV were collected for mRNA quantification.RESULTS:In the RV, acute overload induced IL-6 and TNF-alpha gene expression, higher in VolOv (IL-6: + 669.7 +/- 263.4%; TNF-alpha: + 5149.9 +/- 1099.0%; 360 min) than in PrOv (IL-6: + 64.9 +/- 44.2%; TNF-alpha: + 628.1 +/- 229.3%; 360 min). In PrOv, TNF-alpha mRNA levels in the LV were increased, in the absence of ventricular overload. IL-6 and TNF-alpha mRNA levels did not correlate in the LV, while in the RV a positive correlation was found (r = 0.574; p < 0.001).CONCLUSIONS:Acute cardiac overload induces overexpression of pro-inflammatory cytokines. This gene activation is not uniform, being higher in volume overload and involving both load-dependent and load-independent mechanisms

    Effect of Nonionic Surfactants on the Crystallinity and Thermal Stability of Poly(vinyl alcohol) Film

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    In this study, poly(vinyl alcohol) (PVA)/surfactant films were prepared by casting technique. Two nonionic surfactants with different alkyl chain lenghts (Tween 20 and Tween 40) were used. PVA/Tween 20 and PVA/Tween 40 films were characterized by means of Fourier Transform infrared spectroscopy (FTIR), X-ray diffraction (XRD) and thermogravimetric analysis (TGA). FTIR spectra of PVA/Tween films indicated the presence of hydrogen bond interactions between the Tween surfactants and PVA. XRD results showed that the incorporation of Tween 20 and 40 into the PVA film decreased the crystallinity of PVA.TGA curves revealed an increase in the thermal stability of PVA film in the presence of the surfactants. DOI:&nbsp;http://dx.doi.org/10.17807/orbital.v12i4.151
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