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1.
BMC Pulm Med ; 20(1): 269, 2020 Oct 16.
Artigo em Inglês | MEDLINE | ID: mdl-33066765

RESUMO

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has spread to almost 100 countries, infected over 31 M patients and resulted in 961 K deaths worldwide as of 21st September 2020. The major clinical feature of severe COVID-19 requiring ventilation is acute respiratory distress syndrome (ARDS) with multi-functional failure as a result of a cytokine storm with increased serum levels of cytokines. The pathogenesis of the respiratory failure in COVID-19 is yet unknown, but diffuse alveolar damage with interstitial thickening leading to compromised gas exchange is a plausible mechanism. Hypoxia is seen in the COVID-19 patients, however, patients present with a distinct phenotype. Intracellular levels of nitric oxide (NO) play an important role in the vasodilation of small vessels. To elucidate the intracellular levels of NO inside of RBCs in COVID-19 patients compared with that of healthy control subjects. METHODS: We recruited 14 COVID-19 infected cases who had pulmonary involvement of their disease, 4 non-COVID-19 healthy controls (without pulmonary involvement and were not hypoxic) and 2 hypoxic non-COVID-19 patients subjects who presented at the Masih Daneshvari Hospital of Tehran, Iran between March-May 2020. Whole blood samples were harvested from patients and intracellular NO levels in 1 × 106 red blood cells (RBC) was measured by DAF staining using flow cytometry (FACS Calibour, BD, CA, USA). RESULTS: The Mean florescent of intensity for NO was significantly enhanced in COVID-19 patients compared with healthy control subjects (P ≤ 0.05). As a further control for whether hypoxia induced this higher intracellular NO, we evaluated the levels of NO inside RBC of hypoxic patients. No significant differences in NO levels were seen between the hypoxic and non-hypoxic control group. CONCLUSIONS: This pilot study demonstrates increased levels of intracellular NO in RBCs from COVID-19 patients. Future multi-centre studies should examine whether this is seen in a larger number of COVID-19 patients and whether NO therapy may be of use in these severe COVID-19 patients.


Assuntos
Dióxido de Carbono/metabolismo , Infecções por Coronavirus/metabolismo , Eritrócitos/metabolismo , Hipóxia/metabolismo , Óxido Nítrico/metabolismo , Oxigênio/metabolismo , Pneumonia Viral/metabolismo , Adulto , Idoso , Idoso de 80 Anos ou mais , Doenças Assintomáticas , Betacoronavirus , Gasometria , Estudos de Casos e Controles , Infecções por Coronavirus/sangue , Infecções por Coronavirus/complicações , Feminino , Citometria de Fluxo , Humanos , Hipóxia/sangue , Hipóxia/etiologia , Masculino , Pessoa de Meia-Idade , Pandemias , Pressão Parcial , Projetos Piloto , Pneumonia Viral/sangue , Pneumonia Viral/complicações , Doença Pulmonar Obstrutiva Crônica/sangue , Doença Pulmonar Obstrutiva Crônica/complicações , Doença Pulmonar Obstrutiva Crônica/metabolismo , Vasodilatação , Adulto Jovem
2.
Sensors (Basel) ; 20(17)2020 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-32872310

RESUMO

The non-invasive estimation of blood oxygen saturation (SpO2) by pulse oximetry is of vital importance clinically, from the detection of sleep apnea to the recent ambulatory monitoring of hypoxemia in the delayed post-infective phase of COVID-19. In this proof of concept study, we set out to establish the feasibility of SpO2 measurement from the ear canal as a convenient site for long term monitoring, and perform a comprehensive comparison with the right index finger-the conventional clinical measurement site. During resting blood oxygen saturation estimation, we found a root mean square difference of 1.47% between the two measurement sites, with a mean difference of 0.23% higher SpO2 in the right ear canal. Using breath holds, we observe the known phenomena of time delay between central circulation and peripheral circulation with a mean delay between the ear and finger of 12.4 s across all subjects. Furthermore, we document the lower photoplethysmogram amplitude from the ear canal and suggest ways to mitigate this issue. In conjunction with the well-known robustness to temperature induced vasoconstriction, this makes conclusive evidence for in-ear SpO2 monitoring being both convenient and superior to conventional finger measurement for continuous non-intrusive monitoring in both clinical and everyday-life settings.


Assuntos
Meato Acústico Externo , Hipóxia/diagnóstico , Monitorização Fisiológica/instrumentação , Oximetria/instrumentação , Fotopletismografia/instrumentação , Dispositivos Eletrônicos Vestíveis , Adulto , Betacoronavirus/fisiologia , Infecções por Coronavirus/sangue , Infecções por Coronavirus/diagnóstico , Infecções por Coronavirus/terapia , Estudos de Equivalência como Asunto , Estudos de Viabilidade , Feminino , Dedos , Humanos , Hipóxia/sangue , Masculino , Monitorização Fisiológica/métodos , Oximetria/métodos , Oxigênio/análise , Oxigênio/sangue , Pandemias , Fotopletismografia/métodos , Pneumonia Viral/sangue , Pneumonia Viral/diagnóstico , Pneumonia Viral/terapia , Adulto Jovem
3.
BMC Med ; 18(1): 260, 2020 08 19.
Artigo em Inglês | MEDLINE | ID: mdl-32814566

RESUMO

BACKGROUND: The current target oxygen saturation range for patients with COVID-19 recommended by the National Institutes of Health is 92-96%. MAIN BODY: This article critically examines the evidence guiding current target oxygen saturation recommendation for COVID-19 patients, and raises important concerns in the extrapolation of data from the two studies stated to be guiding the recommendation. Next, it examines the influence of hypoxia on upregulation of ACE2 (target receptor for SARS-CoV-2 entry) expression, with supporting transcriptomic analysis of a publicly available gene expression profile dataset of human renal proximal tubular epithelial cells cultured in normoxic or hypoxic conditions. Finally, it discusses potential implications of specific clinical observations and considerations in COVID-19 patients on target oxygen saturation, such as diffuse systemic endothelitis and microthrombi playing an important pathogenic role in the wide range of systemic manifestations, exacerbation of hypoxic pulmonary vasoconstriction in the setting of pulmonary vascular endothelitis/microthrombi, the phenomenon of "silent hypoxemia" with some patients presenting to the hospital with severe hypoxemia disproportional to symptoms, and overburdened health systems and public health resources in many parts of the world with adverse implications on outpatient monitoring and early institution of oxygen supplementation. CONCLUSIONS: The above factors and analyses, put together, call for an urgent exploration and re-evaluation of target oxygen saturation in COVID-19 patients, both in the inpatient and outpatient settings. Until data from such trials become available, where possible, it may be prudent to target an oxygen saturation at least at the upper end of the recommended 92-96% range in COVID-19 patients both in the inpatient and outpatient settings (in patients that are normoxemic at pre-COVID baseline). Home pulse oximetry, tele-monitoring, and earlier institution of oxygen supplementation for hypoxemic COVID-19 outpatients could be beneficial, where public health resources allow for their implementation.


Assuntos
Betacoronavirus , Infecções por Coronavirus/sangue , Hipóxia/prevenção & controle , Oxigênio/sangue , Pneumonia Viral/sangue , Biomarcadores/sangue , Infecções por Coronavirus/diagnóstico , Infecções por Coronavirus/fisiopatologia , Infecções por Coronavirus/terapia , Humanos , Hipóxia/sangue , Hipóxia/diagnóstico , Hipóxia/etiologia , Oximetria , Pandemias , Pneumonia Viral/diagnóstico , Pneumonia Viral/fisiopatologia , Pneumonia Viral/terapia , Guias de Prática Clínica como Assunto , Telemedicina
4.
Aging (Albany NY) ; 12(16): 15954-15961, 2020 08 19.
Artigo em Inglês | MEDLINE | ID: mdl-32826388

RESUMO

The COVID-19 pandemic has caused monumental mortality, and there are still no adequate therapies. Most severely ill COVID-19 patients manifest a hyperactivated immune response, instigated by interleukin 6 (IL6) that triggers a so called "cytokine storm" and coagulopathy. Hypoxia is also associated with COVID-19. So far overlooked is the fact that both IL6 and hypoxia depress the abundance of a key anticoagulant, Protein S. We speculate that the IL6-driven cytokine explosion plus hypoxemia causes a severe drop in Protein S level that exacerbates the thrombotic risk in COVID-19 patients. Here we highlight a mechanism by which the IL6-hypoxia curse causes a deadly hypercoagulable state in COVID-19 patients, and we suggest a path to therapy.


Assuntos
Infecções por Coronavirus , Síndrome da Liberação de Citocina , Hipóxia , Pandemias , Pneumonia Viral , Proteína S , Trombofilia/imunologia , Anticoagulantes/metabolismo , Anticoagulantes/farmacologia , Betacoronavirus/fisiologia , Infecções por Coronavirus/sangue , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/terapia , Síndrome da Liberação de Citocina/sangue , Síndrome da Liberação de Citocina/virologia , Gerenciamento Clínico , Humanos , Hipóxia/sangue , Hipóxia/etiologia , Hipóxia/imunologia , Interleucina-6/sangue , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/sangue , Pneumonia Viral/imunologia , Pneumonia Viral/terapia , Proteína S/metabolismo , Proteína S/farmacologia , Índice de Gravidade de Doença
6.
PLoS One ; 15(8): e0237673, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32790747

RESUMO

PURPOSE: This study investigated the acute changes in full spectrum differential blood cell count including reticulocytes and immature reticulocytes after a voluntary maximal dry apnea in non-elite divers. Aim of the present study is to obtain information on important regulatory compensation mechanisms and to provide insights into apneic regulatory processes. METHODS: Ten apnea divers performed a voluntary dry mean apnea time of 317 sec [SD ±111 sec]. Differential blood cell count including reticulocytes was measured before and immediately after a single maximal breath-hold. To evaluate kinetics, blood samples were also taken after 30 min and 4 h. Value distributions are presented with dot plots. P-values were calculated using a mixed linear model for time dependency. Four difference values were compared to baseline values with Dunnett's procedure. RESULTS: Significant changes were found in red blood cell parameters for erythrocytes, red cell distribution width, hematocrit, hemoglobin, MCV, reticulocytes and immature reticulocytes, and in white blood cell parameters for leucocytes, lymphocytes, immature granulocytes, monocytes, basophile granulocytes, neutrophil granulocytes and eosinophil granulocytes and for thrombocytes. CONCLUSION: Adaptive mechanisms regarding cell counts in elite apnea divers are not readily transferable to non-elite recreational sportspersons. Divers and physicians should be aware of the limited adaptive performance of humans in the case of extended apnea.


Assuntos
Adaptação Fisiológica/fisiologia , Suspensão da Respiração , Mergulho/fisiologia , Hipóxia/sangue , Adulto , Contagem de Células Sanguíneas , Hematócrito , Hemoglobinas/análise , Humanos , Hipóxia/fisiopatologia , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos
7.
Am J Physiol Lung Cell Mol Physiol ; 319(2): L360-L368, 2020 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-32692577

RESUMO

Hypobaric hypoxia poses stress to sojourners traveling to high-altitude. A cascade of physiological changes occurs to cope with or adapt to hypobaric hypoxia. However, an insufficient physiological response to the hypoxic condition resulting from imbalanced vascular homeostasis pathways results in high-altitude pulmonary edema (HAPE). The present study aims to identify the implication of miRNAs associating with HAPE and adaptation. We analyzed the expression of 1,113 miRNAs in HAPE-patients (HAPE-p), HAPE-free controls (HAPE-f), and highland natives (HLs). Based on miRNA profiling and in silico analyses, miR-124-3p emerged relevantly. We observed a significant overexpression of miR-124-3p in HAPE-p. In silico analyses revealed a direct interaction of miR-124-3p with vascular homeostasis and hypoxia-associated genes NOS3 (endothelial nitric oxide synthase), Apelin, and ETS1 (V-Ets avian erythroblastosis virus E2 oncogene homolog 1). Moreover, the transcript and biolevel expression of these genes were significantly decreased in HAPE-p when compared with HAPE-f or HLs. Our in vitro analysis in human umbilical vein endothelial cells demonstrated a significant knockdown of these genes both at transcript and protein levels following miR-124-3p overexpression. Conclusively, our results showed that miR-124-3p might play a plausible role in HAPE pathophysiology by inhibiting the expression of NOS3, Apelin, and ETS1.


Assuntos
Doença da Altitude/sangue , Doença da Altitude/metabolismo , Hipertensão Pulmonar/sangue , Hipertensão Pulmonar/metabolismo , Hipóxia/sangue , Hipóxia/metabolismo , MicroRNAs/sangue , Edema Pulmonar/sangue , Edema Pulmonar/metabolismo , Adaptação Fisiológica/fisiologia , Adulto , Altitude , Apelina/metabolismo , Linhagem Celular , Feminino , Células HEK293 , Células Endoteliais da Veia Umbilical Humana , Humanos , Masculino , Óxido Nítrico Sintase Tipo III/metabolismo , Proteína Proto-Oncogênica c-ets-1/metabolismo , Adulto Jovem
8.
BMC Infect Dis ; 20(1): 534, 2020 Jul 22.
Artigo em Inglês | MEDLINE | ID: mdl-32698769

RESUMO

BACKGROUND: To analyze the clinical characteristics of Mycoplasma pneumoniae pneumonia with hypoxia in children, and identify the associated risk factors of hypoxia in MPP. METHODS: A retrospective case-control study was performed on 345 children with Mycoplasma pneumoniae pneumonia (MPP) admitted to our hospital wards from January 2017 to June 2019. They were divided into three groups, namely MPP with hypoxia, refractory Mycoplasma pneumoniae pneumonia (RMPP), and general Mycoplasma pneumoniae pneumonia (GMPP). The clinical features, laboratory findings, imaging, and management were collected and compared in the three groups. RESULTS: The MPP with hypoxia patients (n = 69) had longer disease duration, a higher extra-pulmonary complications rate, and more severe radiological abnormalities (P < 0.05). They also needed more complicated treatments (P < 0.05). Meanwhile, the levels of white blood cell count (WBC), C-reactive protein (CRP), lactic dehydrogenase (LDH), interleukin (IL)-6, ferritin, D-dimer, fibrinogen (FG), alanine aminotransferase (ALT) and the percentage of neutrophils in the MPP with hypoxia group were significantly higher than those in the RMPP group and the GMPP group (P < 0.05). In ROC curve analysis, the percentage of neutrophils, WBC, CRP, LDH, IL-6, ferritin, D-dimer, and ALT were contributed to identify the MPP with hypoxia patients. Multivariate logistic regression analysis revealed that ferritin> 174.15 ng/mL, IL-6 > 25.475 pg/ml, and pleural effusion were significantly associated with the incidence of hypoxia in MPP (P < 0.01). CONCLUSION: MPP with hypoxia patients presented more serious clinical manifestations. Ferritin> 174.15 ng/mL, IL-6 > 25.475 pg/ml and pleural effusion were related risk factors for hypoxia in MPP.


Assuntos
Hipóxia/sangue , Hipóxia/complicações , Mycoplasma pneumoniae , Pneumonia por Mycoplasma/sangue , Pneumonia por Mycoplasma/complicações , Proteína C-Reativa/análise , Estudos de Casos e Controles , Criança , Pré-Escolar , Feminino , Ferritinas/sangue , Produtos de Degradação da Fibrina e do Fibrinogênio/análise , Humanos , Interleucina-6/sangue , Contagem de Leucócitos , Masculino , Neutrófilos/metabolismo , Derrame Pleural , Pneumonia por Mycoplasma/microbiologia , Curva ROC , Estudos Retrospectivos , Fatores de Risco
9.
Med Hypotheses ; 143: 110022, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32634734

RESUMO

The current SARS-Cov-2 virus pandemic challenges critical care physicians and other caregivers to find effective treatment for desperately ill patients - especially those with sudden and extreme hypoxemia. Unlike patients with other forms of Acute Respiratory Distress Syndrome, these patients do not exhibit increased lung stiffness or dramatic dyspnea., even in the presence of arterial blood oxygen levels lower than that seen normally in mixed venous blood. Urgent intubation and mechanical ventilation with high inflation pressures and raised inhaled oxygen concentration have proved unhelpful or worse, but why? Our Hypothesis is that sudden opening of a previously undetected probe-patent foramen ovale (PPFO) may explain this mystery. As hypoxemia without acidosis is a rather weak stimulus of dyspnea or increased ventilation, and opening of such an intracardiac shunt would not worsen lung mechanical properties, the absence of dramatic symptom changes would not be surprising. We point out the high frequency of PFO both in life and at autopsy, and the physiological evidence of large shunt fractions found in Covid-19 patients. Published evidence of hypercoagulability and abundant evidence of pulmonary emboli found at autopsy are in accord with our hypothesis, as they would contribute to raised pressure in the pulmonary arteries and right heart chambers, potentially causing a shunt to open. We review the interaction between viral corona spike protein and ACE-2 receptors present on the surface of alveolar lining cells, and contribution to hypercoagulabilty caused by the spike protein. Search for an open PFO after a large drop in arterial oxygen saturation can be performed at the bedside with a variety of well-established techniques including bedside echocardiography, nitrogen washout test, and imaging studies. Potential treatments might include balloon or patch closure of the shunt, and various drug treatments to lower pulmonary vascular resistance.


Assuntos
Betacoronavirus , Infecções por Coronavirus/complicações , Forame Oval Patente/complicações , Hipóxia/etiologia , Pneumonia Viral/complicações , Betacoronavirus/patogenicidade , Betacoronavirus/fisiologia , Infecções por Coronavirus/sangue , Infecções por Coronavirus/fisiopatologia , Forame Oval Patente/sangue , Forame Oval Patente/fisiopatologia , Humanos , Hipóxia/sangue , Hipóxia/fisiopatologia , Modelos Biológicos , Pandemias , Peptidil Dipeptidase A/fisiologia , Pneumonia Viral/sangue , Pneumonia Viral/fisiopatologia , Circulação Pulmonar , Receptores Virais/fisiologia , Mecânica Respiratória , Glicoproteína da Espícula de Coronavírus/fisiologia , Trombofilia/etiologia
11.
Am J Respir Crit Care Med ; 202(3): 356-360, 2020 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-32539537

RESUMO

Patients with coronavirus disease (COVID-19) are described as exhibiting oxygen levels incompatible with life without dyspnea. The pairing-dubbed happy hypoxia but more precisely termed silent hypoxemia-is especially bewildering to physicians and is considered as defying basic biology. This combination has attracted extensive coverage in media but has not been discussed in medical journals. It is possible that coronavirus has an idiosyncratic action on receptors involved in chemosensitivity to oxygen, but well-established pathophysiological mechanisms can account for most, if not all, cases of silent hypoxemia. These mechanisms include the way dyspnea and the respiratory centers respond to low levels of oxygen, the way the prevailing carbon dioxide tension (PaCO2) blunts the brain's response to hypoxia, effects of disease and age on control of breathing, inaccuracy of pulse oximetry at low oxygen saturations, and temperature-induced shifts in the oxygen dissociation curve. Without knowledge of these mechanisms, physicians caring for patients with hypoxemia free of dyspnea are operating in the dark, placing vulnerable patients with COVID-19 at considerable risk. In conclusion, features of COVID-19 that physicians find baffling become less strange when viewed in light of long-established principles of respiratory physiology; an understanding of these mechanisms will enhance patient care if the much-anticipated second wave emerges.


Assuntos
Betacoronavirus , Infecções por Coronavirus/complicações , Infecções por Coronavirus/diagnóstico , Dispneia/virologia , Hipóxia/diagnóstico , Hipóxia/virologia , Pneumonia Viral/complicações , Pneumonia Viral/diagnóstico , Infecções por Coronavirus/sangue , Dispneia/sangue , Dispneia/diagnóstico , Humanos , Hipóxia/sangue , Masculino , Pessoa de Meia-Idade , Oximetria , Oxigênio/sangue , Pandemias , Pneumonia Viral/sangue
13.
PLoS One ; 15(5): e0229753, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32407333

RESUMO

Serum activities of alanine and aspartate aminotransferases (ALT and AST) are used as gold standard biomarkers for the diagnosis of hepatocellular injury. Since ALT and AST lack liver specificity, the diagnosis of the onset of hepatocellular injury in patients with underlying muscle impairments is severely limited. Thus, we evaluated the potential of glutamate dehydrogenase (GLDH) as a liver specific alternative biomarker of hepatocellular injury. In our study, serum GLDH in subjects with Duchene muscular dystrophy (DMD) was equivalent to serum GLDH in age matched healthy subjects, while serum ALT was increased 20-fold in DMD subjects. Furthermore, serum GLDH in 131 subjects with variety of muscle impairments was similar to serum GLDH of healthy subjects while serum ALT corelated with serum creatine kinase, a widely accepted biomarker of muscle impairment. In addition, significant elevations of ALT, AST, and CK were observed in a case of a patient with rhabdomyolysis, while serum GLDH stayed within the normal range until the onset of hypoxia-induced liver injury. In a mouse model of DMD (DMDmdx), serum GLDH but not serum ALT clearly correlated with the degree of acetaminophen-induced liver injury. Taken together, our data support the utility of serum GLDH as a liver-specific biomarker of liver injury that has a potential to improve diagnosis of hepatocellular injury in patients with underlying muscle impairments. In drug development, GLDH may have utility as a biomarker of drug induced liver injury in clinical trials of new therapies to treat muscle diseases such as DMD.


Assuntos
Biomarcadores/sangue , Doença Hepática Induzida por Substâncias e Drogas/sangue , Glutamato Desidrogenase/sangue , Distrofia Muscular de Duchenne/sangue , Acetaminofen/efeitos adversos , Adolescente , Adulto , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Doença Hepática Induzida por Substâncias e Drogas/complicações , Doença Hepática Induzida por Substâncias e Drogas/patologia , Criança , Pré-Escolar , Creatina Quinase/sangue , Modelos Animais de Doenças , Diagnóstico Precoce , Feminino , Humanos , Hipóxia/sangue , Hipóxia/complicações , Fígado/lesões , Fígado/patologia , Masculino , Camundongos , Distrofia Muscular de Duchenne/complicações , Distrofia Muscular de Duchenne/tratamento farmacológico , Distrofia Muscular de Duchenne/patologia , Rabdomiólise/sangue , Rabdomiólise/complicações , Rabdomiólise/patologia
14.
Medicine (Baltimore) ; 99(19): e20031, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32384462

RESUMO

BACKGROUND: It has not been determined that demand valve oxygen therapy is effective for nocturnal hypoxia. A portable oxygen concentrator with an auto-demand oxygen delivery system (auto-DODS; standard, high, and extra high) has recently been developed to improve oxygenation and comfort. This oxygen concentrator can supply a pulsed flow when it detects apnoea. The aim of this study is to demonstrate that this newly developed portable oxygen concentrator with an auto-demand function is non-inferior to a continuous-flow oxygen concentrator for nocturnal hypoxemia. METHODS: Twenty patients with chronic obstructive pulmonary disease or interstitial pneumonia will be randomized to receive a portable oxygen concentrator with an auto-DODS or a continuous-flow oxygen concentrator during sleep. The primary endpoint is mean oxygen saturation (SpO2) during the total sleep time. The secondary endpoints are the ratios of time that the oxygen concentrator spends in each sensitivity mode (standard, high, and extra-high) and at a constant pulse rate to the total sleep time, the total time and ratio of time for which SpO2 is less than 90% during the total sleep time, the lowest value of SpO2 during the total sleep time, the mean and highest pulse rate during the total sleep time, the apnoea index during the total sleep time, the total sleep duration itself, and comfort and reliability as measured by numerical rating scale and questionnaires. DISCUSSION: If the auto-DODS demonstrates non-inferiority to continuous flow in oxygenation during sleep, the auto-DODS can be used even at night, and the patient will need only 1 device. TRIAL REGISTRATION: The study was registered on Aug 23, 2019 (jRCTs052190042).


Assuntos
Hipóxia , Doenças Pulmonares Intersticiais/complicações , Nebulizadores e Vaporizadores , Oxigenoterapia , Doença Pulmonar Obstrutiva Crônica/complicações , Adulto , Estudos Cross-Over , Feminino , Humanos , Hipóxia/sangue , Hipóxia/diagnóstico , Hipóxia/etiologia , Hipóxia/terapia , Masculino , Oximetria/métodos , Oxigenoterapia/instrumentação , Oxigenoterapia/métodos , Polissonografia/métodos , Ensaios Clínicos Controlados Aleatórios como Assunto , Recuperação de Função Fisiológica , Reprodutibilidade dos Testes , Teste de Caminhada/métodos
16.
J Sports Med Phys Fitness ; 60(5): 677-684, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32438783

RESUMO

BACKGROUND: Erythropoietin (EPO) and vascular endothelial growth factor (VEGF) are important factors regulating erythropoiesis and angiogenesis. Altitude/hypoxic training may induce elevated VEGF-A and EPO levels. However, it appears that the range of adaptive changes depends largely on the training method used. Therefore, we investigated the changes in EPO and VEGF-A levels in athletes using three different altitude/hypoxic training concepts. METHODS: Thirty-four male cyclists were randomly divided into four groups: LH-TL group ("live high-train low" protocol), HiHiLo ("live high - base train high - interval train low" procedure), IHT ("intermittent hypoxic training") and control group (CN, normoxic training). The same 4-week training program was used in all groups. Blood samples were taken before and after each training week in order to evaluate serum EPO and VEGF-A levels. RESULTS: In the LH-TL and HiHiLo groups, EPO increased (P<0.001) after 1st week and remained elevated until 3rd week of altitude training. In the IHT and CN groups, EPO did not change significantly. VEGF-A was higher (P<0.001) after 2nd and 3rd week of training in the IHT group. In the HiHiLo group, VEGF-A changed (P<0.05) only after 3rd week. No significant changes of VEGF-A were noted in the LH-TL and CN groups. CONCLUSIONS: Altitude/hypoxic training is effective in increasing VEGF-A and EPO levels. However, a training method plays a key role in the pattern of adaptations. EPO level increase only when an adequate hypoxic dose is provided, whereas VEGF-A increases when the hypoxic exposure is combined with exercise, particularly at high intensity.


Assuntos
Aclimatação/fisiologia , Eritropoetina/sangue , Exercício Físico/fisiologia , Fator A de Crescimento do Endotélio Vascular/sangue , Adulto , Altitude , Humanos , Hipóxia/sangue , Masculino , Adulto Jovem
18.
Artigo em Inglês | MEDLINE | ID: mdl-32267729

RESUMO

We examined the effect of acute intermittent hypoxia (IH) on sympathetic neural firing patterns and the role of the carotid chemoreceptors. We hypothesized exposure to acute IH would increase muscle sympathetic nerve activity (MSNA) via an increase in action potential (AP) discharge rates and within-burst firing. We further hypothesized any change in discharge patterns would be attenuated during acute chemoreceptor deactivation (hyperoxia). MSNA (microneurography) was assessed in 17 healthy adults (11 male/6 female; 31 ± 1 yr) during normoxic rest before and after 30 min of experimental IH. Prior to and following IH, participants were exposed to 2 min of 100% oxygen (hyperoxia). AP patterns were studied from the filtered raw MSNA signal using wavelet-based methodology. Compared with baseline, multiunit MSNA burst incidence (P < 0.01), AP incidence (P = 0.01), and AP content per burst (P = 0.01) were increased following IH. There was an increase in the probability of a particular AP cluster firing once (P < 0.01) and more than once (P = 0.03) per burst following IH. There was no effect of hyperoxia on multiunit MSNA at baseline or following IH (P > 0.05); however, hyperoxia following IH attenuated the probability of particular AP clusters firing more than once per burst (P < 0.01). Acute IH increases MSNA by increasing AP discharge rates and within-burst firing. A portion of the increase in within-burst firing following IH can be attributed to the carotid chemoreceptors. These data advance the mechanistic understanding of sympathetic activation following acute IH in humans.


Assuntos
Corpo Carotídeo/fisiopatologia , Hipóxia/fisiopatologia , Contração Muscular , Músculo Esquelético/inervação , Oxigênio/sangue , Recrutamento Neurofisiológico , Sistema Nervoso Simpático/fisiopatologia , Potenciais de Ação , Adulto , Biomarcadores/sangue , Corpo Carotídeo/metabolismo , Feminino , Humanos , Hipóxia/sangue , Hipóxia/diagnóstico , Masculino , Fatores de Tempo
19.
Ann Neurol ; 87(6): 921-930, 2020 06.
Artigo em Inglês | MEDLINE | ID: mdl-32220084

RESUMO

OBJECTIVE: There is much controversy about the neurobiological mechanisms underlying the effects of sleep-disordered breathing on the brain. The aim of this study was to investigate the association between markers of sleep-related hypoxemia and brain anatomy. METHODS: We used data from a large-scale cohort from the general population (n = 775, 50.6% males, age range = 45-86 years, mean age = 60.3 ± 9.9) that underwent full polysomnography and brain magnetic resonance imaging to correlate respiratory variables with regional brain volume estimates. RESULTS: After adjusting for age, gender, and cardiovascular risk factors, only mean oxygen saturation during sleep was associated with bilateral volume of hippocampus (right: p = 0.001; left: p < 0.001), thalamus (right: p < 0.001; left: p < 0.001), putamen (right: p = 0.001; left: p = 0.001), and angular gyrus (right: p = 0.011; left: p = 0.001). We observed the same relationship in left hemispheric amygdala (p = 0.010), caudate (p = 0.008), inferior frontal gyrus (p = 0.004), and supramarginal gyrus (p = 0.003). The other respiratory variables-lowest oxygen saturation, percentage of sleep time with oxygen saturation < 90%, apnea-hypopnea index, and oxygen desaturation index-did not show any significant association with brain volumes. INTERPRETATION: Lower mean oxygen saturation during sleep was associated with atrophy of cortical and subcortical brain areas known for high sensitivity to oxygen supply. Their vulnerability to hypoxemia may contribute to behavioral phenotype and cognitive decline in patients with sleep-disordered breathing. ANN NEUROL 2020;87:921-930.


Assuntos
Encéfalo/patologia , Oxigênio/sangue , Sono , Adulto , Idoso , Idoso de 80 Anos ou mais , Atrofia , Encéfalo/diagnóstico por imagem , Córtex Cerebral/diagnóstico por imagem , Córtex Cerebral/patologia , Estudos de Coortes , Feminino , Humanos , Hipóxia/sangue , Imagem por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Polissonografia , Respiração , Síndromes da Apneia do Sono/complicações , Transtornos do Sono-Vigília/sangue
20.
Drug Test Anal ; 12(3): 323-330, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31889433

RESUMO

Exposure to either natural or simulated hypoxia induces hematological adaptations that may affect the parameters of the Athlete Biological Passport (ABP). The aim of the present study was to examine the effect of a novel, mixed hypoxic dose protocol on the likelihood of producing an atypical ABP finding. Ten well-trained middle-distance runners participated in a "live high, train low and high" (LHTLH) altitude training camp for 14 days. The participants spent ˜6 hr.d-1 at 3000-5400 m during waking hours and ˜10 h.d-1 overnight at 2400-3000 m simulated altitude. Venous blood samples were collected before (B0), and after 1 (D1), 4 (D4), 7 (D7), and 14 (D14) days of hypoxic exposure, and again 14 days post exposure (P14). Samples were analyzed for key parameters of the ABP including reticulocyte percentage (Ret%), hemoglobin concentration ([Hb]), and the OFF-score. The ABP adaptive model was administered at a specificity of 99% to test for atypical findings. We found significant changes in [Hb] and Ret% during the hypoxic intervention. Consequently, this led to ABP threshold deviations at 99% specificity in three participants. Only one of these was flagged as an "atypical passport finding" (ATPF) due to deviation of the OFF-score. When this sample was evaluated by ABP experts it was considered "normal". In conclusion, it is highly unlikely that the present hypoxic exposure protocol would have led to a citation for a doping violation according to WADA guidelines.


Assuntos
Altitude , Atletas , Doping nos Esportes/métodos , Hipóxia/sangue , Ensino , Adulto , Estudos Cross-Over , Hemoglobinas/metabolismo , Humanos , Masculino , Contagem de Reticulócitos/estatística & dados numéricos , Método Simples-Cego , Fatores de Tempo , Adulto Jovem
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