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1.
Stroke ; 51(10): 3156-3168, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32897811

RESUMO

Understanding the relationship between infection and stroke has taken on new urgency in the era of the coronavirus disease 2019 (COVID-19) pandemic. This association is not a new concept, as several infections have long been recognized to contribute to stroke risk. The association of infection and stroke is also bidirectional. Although infection can lead to stroke, stroke also induces immune suppression which increases risk of infection. Apart from their short-term effects, emerging evidence suggests that poststroke immune changes may also adversely affect long-term cognitive outcomes in patients with stroke, increasing the risk of poststroke neurodegeneration and dementia. Infections at the time of stroke may also increase immune dysregulation after the stroke, further exacerbating the risk of cognitive decline. This review will cover the role of acute infections, including respiratory infections such as COVID-19, as a trigger for stroke; the role of infectious burden, or the cumulative number of infections throughout life, as a contributor to long-term risk of atherosclerotic disease and stroke; immune dysregulation after stroke and its effect on the risk of stroke-associated infection; and the impact of infection at the time of a stroke on the immune reaction to brain injury and subsequent long-term cognitive and functional outcomes. Finally, we will present a model to conceptualize the many relationships among chronic and acute infections and their short- and long-term neurological consequences. This model will suggest several directions for future research.


Assuntos
Aterosclerose/epidemiologia , Infecções/epidemiologia , Acidente Vascular Cerebral/epidemiologia , Arritmias Cardíacas/epidemiologia , Arritmias Cardíacas/fisiopatologia , Aterosclerose/imunologia , Aterosclerose/fisiopatologia , Bacteriemia/epidemiologia , Bacteriemia/imunologia , Bacteriemia/fisiopatologia , Betacoronavirus , Doença Crônica , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/fisiopatologia , Infecções por Citomegalovirus/epidemiologia , Infecções por Citomegalovirus/imunologia , Infecções por Citomegalovirus/fisiopatologia , Endotélio/fisiopatologia , Infecções por HIV/epidemiologia , Infecções por HIV/imunologia , Infecções por HIV/fisiopatologia , Humanos , Hospedeiro Imunocomprometido/imunologia , Infecções/imunologia , Infecções/fisiopatologia , Inflamação/imunologia , Influenza Humana/epidemiologia , Influenza Humana/imunologia , Influenza Humana/fisiopatologia , Pandemias , Ativação Plaquetária , Agregação Plaquetária , Pneumonia/epidemiologia , Pneumonia/imunologia , Pneumonia/fisiopatologia , Pneumonia Viral/epidemiologia , Pneumonia Viral/imunologia , Pneumonia Viral/fisiopatologia , Prognóstico , Fatores de Risco , Acidente Vascular Cerebral/imunologia , Trombose/epidemiologia , Trombose/imunologia , Infecção pelo Vírus da Varicela-Zoster/epidemiologia , Infecção pelo Vírus da Varicela-Zoster/imunologia , Infecção pelo Vírus da Varicela-Zoster/fisiopatologia
3.
Curr Hypertens Rep ; 22(9): 63, 2020 08 27.
Artigo em Inglês | MEDLINE | ID: mdl-32852642

RESUMO

PURPOSE OF REVIEW: To review current literature on endothelial dysfunction with previous coronaviruses, and present available data on the role of endothelial dysfunction in coronavirus disease-2019 (COVID-19) infection in terms of pathophysiology and clinical phenotype RECENT FINDINGS: Recent evidence suggests that signs and symptoms of severe COVID-19 infection resemble the clinical phenotype of endothelial dysfunction, implicating mutual pathophysiological pathways. Dysfunction of endothelial cells is believed to mediate a variety of viral infections, including those caused by previous coronaviruses. Experience from previous coronaviruses has triggered hypotheses on the role of endothelial dysfunction in the pathophysiology of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), which are currently being tested in preclinical and clinical studies. Endothelial dysfunction is the common denominator of multiple clinical aspects of severe COVID-19 infection that have been problematic for treating physicians. Given the global impact of this pandemic, better understanding of the pathophysiology could significantly affect management of patients.


Assuntos
Infecções por Coronavirus/fisiopatologia , Endotélio/fisiopatologia , Pneumonia Viral/fisiopatologia , Betacoronavirus , Células Endoteliais/patologia , Endotélio/virologia , Humanos , Pandemias
4.
Medicine (Baltimore) ; 99(34): e21821, 2020 Aug 21.
Artigo em Inglês | MEDLINE | ID: mdl-32846824

RESUMO

BACKGROUND: Traditional Chinese medicine Tongxinluo (TXL) has been widely used to treat coronary artery disease in China, since it could reduce myocardial infarct size and ischemia/reperfusion injury in both non-diabetic and diabetic conditions. It has been shown that TXL could regulate peroxisome proliferator activated receptor-α (PPAR-α), a positive modulator of angiopoietin-like 4 (Angptl4), in diabetic rats. Endothelial junction substructure components, such as VE-cadherin, are involved in the protection of reperfusion injury. Thus, we hypothesized cell-intrinsic and endothelial-specific Angptl4 mediated the protection of TXL on endothelial barrier under high glucose condition against ischemia/reperfusion-injury via PPAR-α pathway. METHODS: Incubated with high glucose medium, the human cardiac microvascular endothelial cells (HCMECs) were then exposed to oxygen-glucose-serum deprivation (2 hours) and restoration (2 hours) stimulation, with or without TXL, insulin, or rhAngptl4 pretreatment. RESULTS: TXL, insulin, and rhAngptl4 had similar protective effects on the endothelial barrier. TXL treatment reversed the endothelial barrier breakdown in HCMECs significantly as identified by decreasing endothelial permeability, upregulating the expression of JAM-A, VE-cadherin, and integrin-α5 and increasing the membrane location of VE-cadherin and integrin-α5, and these effects of TXL were as effective as insulin and rhAngptl4. However, Angptl4 knock-down with small interfering RNA (siRNA) interference and PPAR-α inhibitor MK886 partially abrogated these beneficial effects of TXL. Western blotting also revealed that similar with insulin, TXL upregulated the expression of Angptl4 in HCMECs, which could be inhibited by Angptl4 siRNA or MK886 exposure. TXL treatment increased PPAR-α activity, which could be diminished by MK886 but not by Angptl4 siRNA. CONCLUSION: These data suggest cell-intrinsic and endothelial-specific Angptl4 mediates the protection of TXL against endothelial barrier breakdown during oxygen-glucose-serum deprivation and restoration under high glucose condition partly via the PPAR-α/Angptl4 pathway.


Assuntos
Proteína 4 Semelhante a Angiopoietina/metabolismo , Medicamentos de Ervas Chinesas/farmacologia , Células Endoteliais/efeitos dos fármacos , Endotélio/efeitos dos fármacos , Endotélio/fisiopatologia , PPAR alfa/metabolismo , Proteína 4 Semelhante a Angiopoietina/genética , Proteína 4 Semelhante a Angiopoietina/farmacologia , Caderinas/metabolismo , Permeabilidade Capilar , Moléculas de Adesão Celular/metabolismo , Células Cultivadas , Vasos Coronários/citologia , Técnicas de Silenciamento de Genes , Glucose/metabolismo , Glucose/farmacologia , Humanos , Indóis/farmacologia , Insulina/farmacologia , Integrina alfa5/metabolismo , Inibidores de Lipoxigenase/farmacologia , Microvasos/citologia , Oxigênio/metabolismo , Oxigênio/farmacologia , Receptores de Superfície Celular/metabolismo , Traumatismo por Reperfusão/metabolismo , Transdução de Sinais
7.
Am J Physiol Endocrinol Metab ; 319(1): E105-E109, 2020 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-32459524

RESUMO

Recent reports have shown a strong association between obesity and the severity of COVID-19 infection, even in the absence of other comorbidities. After infecting the host cells, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may cause a hyperinflammatory reaction through the excessive release of cytokines, a condition known as "cytokine storm," while inducing lymphopenia and a disrupted immune response. Obesity is associated with chronic low-grade inflammation and immune dysregulation, but the exact mechanisms through which it exacerbates COVID-19 infection are not fully clarified. The production of increased amounts of cytokines such as TNFα, IL-1, IL-6, and monocyte chemoattractant protein (MCP-1) lead to oxidative stress and defective function of innate and adaptive immunity, whereas the activation of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome seems to play a crucial role in the pathogenesis of the infection. Endothelial dysfunction and arterial stiffness could favor the recently discovered infection of the endothelium by SARS-CoV-2, whereas alterations in cardiac structure and function and the prothrombotic microenvironment in obesity could provide a link for the increased cardiovascular events in these patients. The successful use of anti-inflammatory agents such as IL-1 and IL-6 blockers in similar hyperinflammatory settings, like that of rheumatoid arthritis, has triggered the discussion of whether such agents could be administrated in selected patients with COVID-19 disease.


Assuntos
Infecções por Coronavirus/fisiopatologia , Obesidade/virologia , Pneumonia Viral/fisiopatologia , Imunidade Adaptativa , Betacoronavirus , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/metabolismo , Síndrome da Liberação de Citocina/virologia , Endotélio/fisiopatologia , Coração/fisiopatologia , Coração/virologia , Humanos , Imunidade Inata , Inflamação , Proteína 3 que Contém Domínio de Pirina da Família NLR/imunologia , Estresse Oxidativo , Pandemias , Pneumonia Viral/imunologia , Pneumonia Viral/metabolismo , Fatores de Risco , Trombose/fisiopatologia , Rigidez Vascular
8.
J Womens Health (Larchmt) ; 29(6): 770-779, 2020 06.
Artigo em Inglês | MEDLINE | ID: mdl-32074468

RESUMO

Microvascular disease, or small-vessel disease, is a multisystem disorder with a common pathophysiological basis that differentially affects various organs in some patients. The prevalence of small-vessel disease in the heart has been found to be higher in women compared with men. Additionally, other diseases prominently affecting women, including heart failure with preserved ejection fraction, Takotsubo cardiomyopathy, cerebral small-vessel disease, preeclampsia, pulmonary arterial hypertension (PAH), endothelial dysfunction in diabetes, diabetic cardiomyopathy, rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis, may have a common etiologic linkage related to microvascular disease. To the best of our knowledge this is the first article to investigate this potential linkage. We sought to identify various diseases with a shared pathophysiology involving microvascular/endothelial dysfunction that primarily affect women, and their potential implications for disease management. Advanced imaging technologies, such as magnetic resonance imaging and positron-emission tomography, enable the detection and increased understanding of microvascular dysfunction in various diseases. Therapies that improve endothelial function, such as those used in PAH, may also be associated with benefits across the full spectrum of microvascular dysfunction. A shared pathology across multiple organ systems highlights the need for a collaborative, multidisciplinary approach among medical subspecialty practitioners who care for women with small-vessel disease. Such an approach may lead to accelerated research in diseases that affect women and their quality of life.


Assuntos
Endotélio/fisiopatologia , Doenças Vasculares/fisiopatologia , Doença da Artéria Coronariana/fisiopatologia , Circulação Coronária , Diabetes Mellitus/fisiopatologia , Feminino , Insuficiência Cardíaca , Humanos , Lúpus Eritematoso Sistêmico/fisiopatologia , Qualidade de Vida , Fatores de Risco
9.
Crit Care Med ; 48(3): 344-352, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-32058372

RESUMO

OBJECTIVES: Systemic endothelial activation may contribute to sepsis-associated organ injury, including acute respiratory distress syndrome. We hypothesized that children with extrapulmonary sepsis with versus without acute respiratory distress syndrome would have plasma biomarkers indicative of increased endothelial activation and that persistent biomarker changes would be associated with poor outcome. DESIGN: Observational cohort. SETTING: Academic PICU. PATIENTS: Patients less than 18 years old with sepsis from extrapulmonary infection with (n = 46) or without (n = 54) acute respiratory distress syndrome and noninfected controls (n = 19). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Endothelial (angiopoietin-1, angiopoietin-2, tyrosine kinase with immunoglobulin-like loop epidermal growth factor homology domain 2, vascular endothelial growth factor, soluble fms-like tyrosine kinase, von Willebrand factor, E-selectin, intercellular adhesion molecule, vascular cell adhesion molecule, thrombomodulin) and inflammatory biomarkers (C-reactive protein, interleukin-6, and interleukin-8) were measured from peripheral plasma collected within 3 days (time 1) of sepsis recognition and at 3-6 days (time 2) and 7-14 days (time 3). Time 1 biomarkers and longitudinal measurements were compared for sepsis patients with versus without acute respiratory distress syndrome and in relation to complicated course, defined as greater than or equal to two organ dysfunctions at day 7 or death by day 28. Angiopoietin-2, angiopoietin-2/angiopoietin-1 ratio, tyrosine kinase with immunoglobulin-like loop epidermal growth factor homology domain 2, vascular endothelial growth factor, von Willebrand factor, E-selectin, intercellular adhesion molecule, vascular cell adhesion molecule, thrombomodulin, endocan, C-reactive protein, interleukin-6, and interleukin-8 were different between sepsis and noninfected control patients at time 1. Among patients with sepsis, those with acute respiratory distress syndrome had higher angiopoietin-2/angiopoietin-1 ratio, vascular endothelial growth factor, vascular cell adhesion molecule, thrombomodulin, endocan, interleukin-6, and interleukin-8 than those without acute respiratory distress syndrome (all p < 0.003). Angiopoietin-2 and angiopoietin-2/angiopoietin-1 ratio remained higher in sepsis with versus without acute respiratory distress syndrome after multivariable analyses. Time 1 measures of angiopoietin-2, angiopoietin-2/-1 ratio, von Willebrand factor, and endocan were indicative of complicated course in all sepsis patients (all area under the receiver operating curve ≥ 0.80). In sepsis without acute respiratory distress syndrome, soluble fms-like tyrosine kinase decreased more quickly and von Willebrand factor and thrombomodulin decreased more slowly in those with complicated course. CONCLUSIONS: Children with extrapulmonary sepsis with acute respiratory distress syndrome had plasma biomarkers indicative of greater systemic endothelial activation than those without acute respiratory distress syndrome. Several endothelial biomarkers measured near sepsis recognition were associated with complicated course, whereas longitudinal biomarker changes yielded prognostic information only in those without sepsis-associated acute respiratory distress syndrome.


Assuntos
Endotélio/fisiopatologia , Unidades de Terapia Intensiva Pediátrica/estatística & dados numéricos , Sepse/epidemiologia , Sepse/fisiopatologia , Adolescente , Biomarcadores , Proteínas Sanguíneas/metabolismo , Moléculas de Adesão Celular/metabolismo , Criança , Pré-Escolar , Feminino , Mortalidade Hospitalar , Humanos , Lactente , Mediadores da Inflamação , Estudos Longitudinais , Masculino , Escores de Disfunção Orgânica , Prognóstico , Sepse/sangue , Fatores de Tempo
10.
Clin Exp Hypertens ; 42(1): 24-30, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-30626217

RESUMO

The isometric handgrip training (IHT) has been emerging as an alternative approach for blood pressure (BP) reduction in hypertensive patients. However, the mechanisms underlying the reductions in BP after IHT are poorly known. Thus, the aim of this study was to analyze the vascular effects of IHT in hypertensive patients. A randomized controlled trial was conducted with 33 hypertensive patients (61 ± 2 y.o.; 67% female) who were randomly assigned to two groups: IHT or control group. The IHT group has completed three weekly sessions of isometric handgrip (4 × 2 â€Šmin sets, alternating the hands at 30% of maximal voluntary contraction). Before and after a period of 12 weeks BP, arterial stiffness, central and peripheral pulse wave velocity (PWV) and endothelial function were measured. The IHT approach has significantly decreased systolic (∆ = -16 ± 2 vs. ∆ = -3 ± 3 mmHg, p < 0.001) and diastolic (∆ = -8 ± 2 vs. ∆ = 0 ± 2 mmHg, p = 0.014) BP. Reductions in central PWV (IHT: 9.1 ± 0.5 vs. 8.0 ± 0.3 m/s; Control: 8.8 ± 0.5 m/s, p < 0.05) and shear rate area after occlusion have significantly reduced by using the IHT (37822 ± 6931 vs. 24829 ± 5337 s-1, p < 0.05). In conclusion, 12 weeks of IHT have reduced the BP and arterial stiffness and improved markers of endothelial function in hypertensive patients.


Assuntos
Endotélio/fisiopatologia , Exercício Físico/fisiologia , Força da Mão/fisiologia , Hipertensão/fisiopatologia , Pressão Sanguínea , Feminino , Humanos , Contração Isométrica , Masculino , Pessoa de Meia-Idade , Análise de Onda de Pulso , Treinamento de Resistência , Rigidez Vascular
11.
Respirology ; 25(1): 89-96, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-30985946

RESUMO

BACKGROUND AND OBJECTIVE: Chronic lung disease is associated with impaired endothelial function and this may be a risk factor for poor cardiovascular health. It is unknown if there is an association between lung and endothelial function in the general population. We investigated associations between lung and endothelial function in a population-based cohort of 38-year-old men and women. METHODS: Systemic endothelial function was measured using peripheral arterial tonometry to calculate the Framingham reactive hyperaemia index. Lung function was assessed using spirometry, plethysmographic lung volumes, airway conductance and gas transfer. Associations between lung and endothelial function were assessed with and without adjustment for potential confounding factors using regression analyses. RESULTS: Sex modified the association between lung and endothelial function. Among women, lower values of pre- and post-bronchodilator spirometry, total lung capacity and functional residual capacity (FRC) were associated with worse endothelial function (P < 0.05). These associations persisted after adjustment for smoking, asthma diagnoses, fitness and body mass index. Associations were weaker among men: only FRC, airway conductance and post-bronchodilator forced expiratory volume in 1 s (FEV1 )/forced vital capacity (FVC) ratios were associated with endothelial function. Endothelial function was not associated with gas transfer in either sex. CONCLUSION: Lower lung volumes and airflow obstruction are associated with endothelial dysfunction among women. There is weaker evidence for an association between airway and endothelial function in men. These findings may partly explain the increased risk of cardiovascular disease among people with poor lung function, but suggest that there are sex differences in this association.


Assuntos
Endotélio/fisiopatologia , Pulmão/fisiopatologia , Adulto , Artérias/fisiopatologia , Estudos de Coortes , Feminino , Volume Expiratório Forçado , Capacidade Residual Funcional , Humanos , Masculino , Manometria , Fatores Sexuais , Espirometria , Capacidade Vital
12.
Chest ; 157(3): 673-685, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31542452

RESUMO

Patients with chronic kidney disease have increased morbidity and mortality, mainly due to cardiovascular disease. Compared with the general population, patients with chronic kidney disease have an increased prevalence of both OSA and central sleep apnea, and the presence of sleep apnea in this population has been associated with an increased risk of cardiovascular events and mortality. Although OSA can lead to an increase in the rate of kidney function decline, there is also evidence that the presence of end-stage renal disease can lead to worsening of sleep apnea, indicating a bidirectional relation between sleep apnea and chronic kidney disease. The objective of this review was to describe the epidemiology of sleep apnea in chronic kidney disease, understand the pathophysiological mechanisms by which OSA can lead to progression of chronic kidney disease, and consider the role of treatment with CPAP in this regard. The review also explores the pathophysiological mechanism by which end-stage renal disease can lead to sleep apnea and considers how intensification of renal replacement therapy or extra fluid removal by ultrafiltration may attenuate the degree of sleep apnea severity in this population.


Assuntos
Falência Renal Crônica/epidemiologia , Insuficiência Renal Crônica/epidemiologia , Apneia do Sono Tipo Central/epidemiologia , Apneia Obstrutiva do Sono/epidemiologia , Pressão Positiva Contínua nas Vias Aéreas , Progressão da Doença , Endotélio/fisiopatologia , Humanos , Hipertensão/fisiopatologia , Hipóxia/metabolismo , Hipóxia/fisiopatologia , Inflamação , Falência Renal Crônica/fisiopatologia , Falência Renal Crônica/terapia , Estresse Oxidativo/fisiologia , Insuficiência Renal Crônica/metabolismo , Insuficiência Renal Crônica/fisiopatologia , Terapia de Substituição Renal , Sistema Renina-Angiotensina/fisiologia , Apneia do Sono Tipo Central/fisiopatologia , Apneia Obstrutiva do Sono/metabolismo , Apneia Obstrutiva do Sono/fisiopatologia , Apneia Obstrutiva do Sono/terapia , Sistema Nervoso Simpático/fisiopatologia , Rigidez Vascular
13.
Arch Ital Biol ; 158(2): 37-44, 2020 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-33462797

RESUMO

This study was aimed to examine the effects of caffeic acid phenethyl ester (CAPE) on endothelial dysfunction in rats with exercise-induced oxidative stress. Tests were performed on male (n=32) young adult Sprague-Dawley rats (12 weeks of age). The experimental animals were divided into four groups in equal numbers. Group 1: General control group; Group 2: Swimming control group. Group 3: CAPE supplemented general control group. Group 4: CAPE supplemented swimming group. Furthermore, animals used in the experiment were made to do exhaustion practice toward the end of the examination. Plasma and liver tissue asymmetric dimethylarginine (ADMA) concentrations were not significantly (p0.05) increased in rats with acute swimming exercise compared to controls. Blood and liver cytokines levels were expanded in comparison to control group and CAPE groups (p0.05). Total antioxidant status (TAS) levels in acute swimming exercise groups reduced compared to the control group. Besides, total oxidant status (TOS) levels were considerably elevated compared to the control and CAPE groups. In this study, acute swimming exercise induced that oxidative stress could cause early onset of endothelial damage. Besides, CAPE can demonstrate protective effects on endothelial damage, inflammation and oxidative stress axis.


Assuntos
Ácidos Cafeicos/farmacologia , Endotélio/efeitos dos fármacos , Endotélio/fisiopatologia , Estresse Oxidativo , Álcool Feniletílico/análogos & derivados , Condicionamento Físico Animal/efeitos adversos , Animais , Antioxidantes/fisiologia , Inflamação , Masculino , Álcool Feniletílico/farmacologia , Ratos , Ratos Sprague-Dawley
14.
Zh Nevrol Psikhiatr Im S S Korsakova ; 119(8. Vyp. 2): 46-52, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31825362

RESUMO

AIM: To study the changes in endothelial dysfunction and von Willebrand factor activity in acute and chronic stages of hemispheric intracerebral hemorrhage (ICH) and their influence on clinical severity and functional recovery. MATERIAL AND METHODS: Fifty patients with hemispheric ICH, aged 61.6±11.2 years, and 30 patients with AH, aged 59.6±6.2 years, (comparison group) were examined. Patients with ICH were examined on admission, 6-8th, 13-15th days, and 11.1±0.9 months after stroke onset. Patients with arterial hypertension (AH) were examined on admission. Changes in NIHSS, Glasgow coma scale, and modified Rankin scale were studied. Restocetin induced platelet aggregation (RIPA) was assessed by optical aggregometry (BIOLA LA230-2 AGGRWB) in modification by G. Born and Z. Gabbasov. von Willebrand factor (vWF) activity was examined as described by J. Olson. RESULTS: RIPA was significantly higher in acute ICH compared to chronic ICH, AH and reference values. RIPA values were negatively correlated with hematoma volume and midline shift (r≥ -0.308, p≤0.035). vWF activity was significantly higher in ICH patients than in AH and reference values. Patients with AH also had significantly higher vWF activity than reference values. In acute ICH, vWF activity steadily increased reaching maximal values by 13-15th day. In chronic ICH, vWF activity decreased compared to the acute phase, but still remained higher than in AH patients or reference values. In acute phase, 1% increment in vWF values resulted in 0.5% increase in the risk of death during the follow-up period (95% CI 1.001-1.008, p=0.007). CONCLUSION: Endothelial dysfunction assessed by vWF activity increases during the acute hemispheric ICH and remains elevated in the chronic stage. vWF activity may be used as a marker in assessing stroke outcome and prognosis.


Assuntos
Hemorragia Cerebral , Endotélio , Acidente Vascular Cerebral , Fator de von Willebrand , Idoso , Hemorragia Cerebral/diagnóstico , Endotélio/fisiopatologia , Humanos , Pessoa de Meia-Idade , Agregação Plaquetária , Prognóstico
15.
Adv Chronic Kidney Dis ; 26(6): 417-426, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31831120

RESUMO

The increase in prevalence and severity of vascular calcification in chronic kidney disease is a result of complex interactions between changes in the vascular bed, mineral metabolites, and other uremic factors. Vascular calcification can occur in the intima and the media of arterial wall. Under permissive conditions, vascular smooth muscle cells (VSMCs) can transform to osteoblast-like phenotype. The membrane-bound vesicles released from transformed VSMCs and the apoptotic bodies derived from dying VSMCs serve as nucleating structures for calcium crystal formation. Alterations in the quality and the quantity of endogenous calcification inhibitors also give rise to an environment that potentiates calcification.


Assuntos
Aterosclerose/metabolismo , Miócitos de Músculo Liso/fisiologia , Insuficiência Renal Crônica/metabolismo , Calcificação Vascular/metabolismo , Animais , Aterosclerose/etiologia , Proteínas de Ligação ao Cálcio/metabolismo , Transdiferenciação Celular , Endotélio/fisiopatologia , Proteínas da Matriz Extracelular/metabolismo , Humanos , Magnésio/metabolismo , Insuficiência Renal Crônica/complicações , Túnica Íntima/patologia , Calcificação Vascular/etiologia , alfa-2-Glicoproteína-HS/metabolismo
16.
Zh Nevrol Psikhiatr Im S S Korsakova ; 119(11): 133-138, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31851185

RESUMO

Endothelial dysfunction today is recognized as one of the leading factors in the pathogenesis of diseases of the central nervous system of various etiologies. Numerous studies have shown the role of hyperhomocysteinemia in the development of endothelial dysfunction and prothrombogenic state. The most important condition in the development of multiple sclerosis (MS) is dysregulation of the blood-brain barrier (BBB) and transendothelial leukocyte migration. It has been proven that homocysteine also contributes to the damage of neurons by the mechanism of excitotoxicity and induction of apoptosis of neurons. These processes can be one of the factors of neurodegenerative brain damage, which plays a leading role in the progression of MS. This review describes the pleiotropic effect of homocysteine on these processes and its role in the pathogenesis of MS.


Assuntos
Endotélio , Hiper-Homocisteinemia , Esclerose Múltipla , Barreira Hematoencefálica , Sistema Nervoso Central , Endotélio/fisiopatologia , Humanos , Hiper-Homocisteinemia/imunologia , Hiper-Homocisteinemia/fisiopatologia , Esclerose Múltipla/imunologia , Esclerose Múltipla/fisiopatologia , Neurônios
17.
Rev Soc Bras Med Trop ; 52: e20180353, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31778418

RESUMO

INTRODUCTION: Dengue is an important mosquito-borne disease in tropical and subtropical regions. Adhesion molecules have not been systematically characterized in the renal tissue of patients with severe dengue (SD). The objective of this study was to detect viral antigens in samples from patients that evolved with SD, correlating with the expression of ICAM-1, VCAM-1, VE-cadherin, and E-selectin to contribute to a better understanding of the pathophysiology of SD. METHODS: Kidney specimens from patients with SD were selected according to clinical and laboratorial data and submitted to histological and immunohistochemistry analysis. A semiquantitative evaluation was performed considering positive immunostaining in 20 glomeruli. RESULTS: Viral antigens were mainly detected in distal tubules. The intense immunostaining of VCAM-1 and ICAM-1 was observed. The expression of E-selectin was discrete, and VE-cadherin expression varied from mild to moderate. VCAM-1 was slightly intense in the glomerular capsule; the expression of ICAM-1 was diffuse. E-selectin was diffuse, and VE-cadherin varied from mild to moderate. The most frequent histological findings were glomerular congestion, mild glomerulitis, acute renal injury, and glomerular atrophy. CONCLUSIONS: The results appear to demonstrate an imbalance between vascular endothelial permeability regulating events in renal lesions in SD. The increase in the expression of ICAM-1 and VCAM-1 is an in-situ indicator of higher permeability with a consequent influx of cells favoring the inflammation of the endothelium. These molecules are important in the pathophysiology of the disease and provide the possibility of developing new markers for the evaluation, clinical follow-up, and therapeutic response of patients with SD.


Assuntos
Selectina E/fisiologia , Endotélio/fisiopatologia , Molécula 1 de Adesão Intercelular/fisiologia , Dengue Grave/sangue , Dengue Grave/fisiopatologia , Molécula 1 de Adesão de Célula Vascular/fisiologia , Adolescente , Adulto , Antígenos CD/sangue , Antígenos CD/fisiologia , Antígenos Virais/sangue , Biomarcadores/sangue , Caderinas/sangue , Caderinas/fisiologia , Criança , Pré-Escolar , Progressão da Doença , Selectina E/sangue , Feminino , Humanos , Imuno-Histoquímica , Molécula 1 de Adesão Intercelular/sangue , Masculino , Pessoa de Meia-Idade , Regulação para Cima , Molécula 1 de Adesão de Célula Vascular/sangue , Adulto Jovem
19.
Sci Total Environ ; 694: 133674, 2019 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-31756800

RESUMO

Exposure to fine particulate matter (PM2.5) can result in adverse cardiovascular responses including vascular endothelial dysfunction, whereas exercise training can promote cardiovascular health. However, whether exercise training can mitigate adverse vascular response to PM2.5 has been less studied. In the present study, we aimed to investigate the preventive effect of exercise training on vascular endothelial dysfunction induced by PM2.5 instillation. Six-week old male Wistar rats (n = 32) were divided into four groups (8 rats per group) by exercise status (sedentary vs. exercised) and PM2.5 exposure (instilled vs. non-instilled). Rats received treadmill training with moderate-intensity intervals in week 1 to 6, followed by three repeated PM2.5 instillation on every other day in week 7. Body weight and blood pressure were measured for each rat regularly during exercise training and before sacrifice. At sacrifice, thoracic aortas were isolated for functional response measurement to agonists. Nitric oxide bioavailability and high-density lipoprotein (HDL) function were also assessed. We observed that exercise training significantly reduced the body weight of rats, while PM2.5 instillation had little effect. Neither exercise training nor PM2.5 instillation had significant effects on blood pressure changes. However, exercise training effectively prevented endothelium-dependent vasorelaxation dysfunction and nitric oxide bioavailability reduction from subsequent PM2.5 instillation. In addition, exercise training promoted HDL function which were characterized as increased HDL cholesterol level, cholesterol efflux capacity, and reduced oxidization index; whereas PM2.5 instillation showed limited adverse impact on HDL function. Collectively, our results indicated that exercise training could promote HDL function and protect against endothelium dysfunction from PM2.5 instillation.


Assuntos
Poluentes Atmosféricos/toxicidade , Endotélio/efeitos dos fármacos , Material Particulado/toxicidade , Animais , Endotélio/fisiopatologia , Masculino , Ratos , Ratos Wistar , Testes de Toxicidade
20.
JAMA Netw Open ; 2(10): e1913615, 2019 10 02.
Artigo em Inglês | MEDLINE | ID: mdl-31626317

RESUMO

Importance: Human immunodeficiency virus (HIV) infection is associated with increased cardiovascular disease (CVD) events. Endothelial dysfunction (EDF) is involved in CVD pathogenesis; however, EDF onset after HIV acquisition and the potential for reversibility with antiretroviral therapy (ART) have not been evaluated to date. Objective: To evaluate endothelial function with noninvasive reactive hyperemia index (RHI) in patients with early HIV infection at baseline and after ART initiation. Design, Setting, and Participants: Cohort study in which 61 members of the United States Air Force diagnosed with HIV infection from September 1, 2015, through September 30, 2017, were evaluated for baseline EDF. Natural log-transformed RHI values (lnRHI) of less than 0.51 and at least 0.51 were defined as abnormal and normal, respectively. The RHI interval changes were evaluated in a subgroup of 40 patients. Data were analyzed from September 30, 2017, through January 30, 2018. Exposure: Early HIV infection. Main Outcomes and Measures: Baseline EDF at HIV diagnosis and interval changes associated with ART initiation. Results: The 61 patients included in the analysis were predominantly male (58 [95%]) and mostly African American (35 [57%]), with a mean (SD) age of 28.1 (6.7) years at HIV diagnosis. Median time from estimated date of HIV seroconversion to RHI assessment was 10.6 months (interquartile range [IQR], 5.1-13.2 months), and the median CD4 lymphocyte count was 552/µL (IQR, 449/µL-674/µL). Patients had a mean (SD) body mass index of 26.2 (4.0), median (IQR) low-density lipoprotein cholesterol level of 97 (80-126) mg/dL, median (IQR) total cholesterol level of 163 (146-195) mg/dL, and no diabetes diagnoses. Overall mean (SD) lnRHI was 0.70 (0.29) at HIV diagnosis. Baseline RHI was normal in 47 patients (77%; mean [SD] lnRHI, 0.82 [0.20]) and was abnormal in 14 patients (23%; mean [SD] lnRHI, 0.30 [0.18]). Age (per 10-year increase) was not associated with an abnormal lnRHI (odds ratio, 2.15; 95% CI, 0.89-5.19; P = .09). Of the 41 patients with follow-up RHI assessments, 40 started ART immediately and repeated the RHI assessments at a median (IQR) of 6.4 (6.0-7.8) months. Use of ART was associated with an overall significan increase in mean (SD) lnRHI (0.13 [0.33]; P = .02). A greater increase in mean (SD) lnRHI was associated with abnormal (n = 11) compared with normal (n = 29) lnRHI at HIV diagnosis (0.33 [0.34]; P = .01 vs 0.04 [0.30]; P = .38). Among those with abnormal baseline lnRHI, 8 (73%) showed improved endothelial function after ART. The patient who declined ART converted from having a normal lnRHI (0.60) to an abnormal lnRHI (0.11) lnRHI after 8.3 months. Conclusions and Relevance: In this study, EDF was common in early HIV infection, with associated reversal in most patients taking ART. Results suggest that persistent EDF and CVD complications may be associated with delayed ART. Further studies are necessary to define the role of noninvasive endothelial function testing in patients with HIV infection.


Assuntos
Fármacos Anti-HIV/uso terapêutico , Endotélio/fisiopatologia , Infecções por HIV/tratamento farmacológico , Hiperemia/virologia , Adulto , Contagem de Linfócito CD4 , Feminino , Infecções por HIV/complicações , Infecções por HIV/imunologia , Humanos , Masculino , Fatores de Tempo , Adulto Jovem
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