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4.
Thorax ; 76(7): 704-713, 2021 07.
Article in English | MEDLINE | ID: covidwho-1322844

ABSTRACT

BACKGROUND: Poor sleep may contribute to chronic kidney disease (CKD) through several pathways, including hypoxia-induced systemic and intraglomerular pressure, inflammation, oxidative stress and endothelial dysfunction. However, few studies have investigated the association between multiple objectively measured sleep dimensions and CKD. METHODS: We investigated the cross-sectional association between sleep dimensions and CKD among 1895 Multi-Ethnic Study of Atherosclerosis Sleep Ancillary Study participants who completed in-home polysomnography, wrist actigraphy and a sleep questionnaire. Using Poisson regression models with robust variance, we estimated separate prevalence ratios (PR) and 95% CIs for moderate-to-severe CKD (glomerular filtration rate <60 mL/min/1.73 m2 or albuminuria >30 mg/g) among participants according to multiple sleep dimensions, including very short (≤5 hours) sleep, Apnoea-Hypopnoea Index and sleep apnoea-specific hypoxic burden (SASHB) (total area under the respiratory event-related desaturation curve divided by total sleep duration, %min/hour)). Regression models were adjusted for sociodemographic characteristics, health behaviours and clinical characteristics. RESULTS: Of the 1895 participants, mean age was 68.2±9.1 years, 54% were women, 37% were white, 28% black, 24% Hispanic/Latino and 11% Asian. Several sleep metrics were associated with higher adjusted PR of moderate-to-severe CKD: very short versus recommended sleep duration (PR=1.40, 95% CI 1.06 to 1.83); SASHB (Box-Cox transformed SASHB: PR=1.06, 95% CI 1.02 to 1.12); and for participants in the highest quintile of SASHB plus sleep apnoea: PR=1.28, 95% CI 1.01 to 1.63. CONCLUSIONS: Sleep apnoea associated hypoxia and very short sleep, likely representing independent biological mechanisms, were associated with a higher moderate-to-severe CKD prevalence, which highlights the potential role for novel interventions.


Subject(s)
Atherosclerosis/complications , Hypoxia/etiology , Renal Insufficiency, Chronic/complications , Sleep Apnea Syndromes/complications , Sleep/physiology , Actigraphy , Aged , Aged, 80 and over , Atherosclerosis/ethnology , Cross-Sectional Studies , Female , Humans , Hypoxia/physiopathology , Male , Middle Aged , Polysomnography , Prevalence , Renal Insufficiency, Chronic/ethnology , Risk Factors , Self Report , Sleep Apnea Syndromes/ethnology , Sleep Apnea Syndromes/physiopathology , United States/epidemiology
5.
Auton Neurosci ; 235: 102842, 2021 11.
Article in English | MEDLINE | ID: covidwho-1293578

ABSTRACT

Coronavirus-19 (COVID-19), the infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, has wreaked havoc across the globe since its emergence in December 2019. Reports of patients presenting with syncope and pre-syncope, as well as hypoxemia without symptoms of dyspnea ("silent hypoxemia"), have led researchers to speculate whether SARS-CoV-2 can alter autonomic nervous system function. As viral infections are commonly reported triggers of altered autonomic control, we must consider whether SARS-CoV-2 can also interfere with autonomic activity, at least in some patients. As we are still in the early stages of understanding COVID-19, we still do not know whether syncope and silent hypoxemia are more strongly associated with COVID-19 compared to any other viral infections that severely compromise gas exchange. Therefore, in this perspective we discuss these two intriguing clinical presentations, as they relate to autonomic nervous system function. In our discussion, we will explore COVID-specific, as well as non-COVID specific mechanisms that may affect autonomic activity and potential therapeutic targets. As we move forward in our understanding of COVID-19, well-designed prospective studies with appropriate control and comparator groups will be necessary to identify potential unique effects of COVID-19 on autonomic function.


Subject(s)
Autonomic Nervous System Diseases/complications , COVID-19/complications , Hypoxia/complications , Syncope/complications , Autonomic Nervous System Diseases/physiopathology , COVID-19/physiopathology , Humans , Hypoxia/physiopathology , Syncope/physiopathology
6.
J Aerosol Med Pulm Drug Deliv ; 34(4): 262-264, 2021 08.
Article in English | MEDLINE | ID: covidwho-1276115

ABSTRACT

Despite the various parenchymal presentation of coronavirus disease 2019 (COVID-19) pneumonia, the involvement of the vascular component, the reduction of perfusion in noninjured part of the lung and secondary right to left shunt play an important role in the genesis of the respiratory insufficiency. We present the case of a 72-year-old woman admitted to Livorno Hospital for severe respiratory insufficiency due to SARS-CoV-2 infection unresponsive to noninvasive in whom administration of nebulized phosphodiesterase 3 (PDE3) inhibitor enoximone was able to improve oxygenation avoiding tracheal intubation. Intravenous infusions of phosphodiesterase inhibitors are commonly used as pulmonary vasodilators in the management of pulmonary hypertension. This is the first case showing that inhaled route administration of PDE3 inhibitor enoximone could be important in the management of COVID-19 hypoxemia, to restore perfusion in noninjured part of the lung, improving oxygenation and avoiding risks of systemic infusion.


Subject(s)
COVID-19/drug therapy , Enoximone/administration & dosage , Hypoxia/drug therapy , Lung/blood supply , Phosphodiesterase 3 Inhibitors/administration & dosage , Pulmonary Circulation/drug effects , Administration, Inhalation , Aerosols , Aged , COVID-19/physiopathology , COVID-19/virology , Female , Humans , Hypoxia/physiopathology , Hypoxia/virology , Nebulizers and Vaporizers , Treatment Outcome
8.
Med Hypotheses ; 146: 110421, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-1233540

ABSTRACT

BACKGROUND: Infection with SARS-CoV-2 is responsible for the COVID-19 crisis affecting the whole world. This virus can provoke acute respiratory distress syndrome (ARDS) leading to overcrowed the intensive care unit (ICU). Over the last months, worldwide experience demonstrated that the ARDS in COVID-19 patients are in many ways "atypical". The mortality rate in ventilated patients is high despite the application of the gold standard treatment (protective ventilation, curare, prone position, inhaled NO). Several studies suggested that the SARS-CoV-2 could interact negatively on red blood cell homeostasis. Furthermore, SarsCov2 creates Reactive Oxygen Species (ROS), which are toxic and generate endothelial dysfunction. Hypothesis/objective(s) We hypothesis that HEMO2Life® administrated intravenously is safe and could help symptomatically the patient condition. It would increase arterial oxygen content despite lung failure and allow better tissue oxygenation control. The use of HEMO2Life® is also interesting due to its anti-oxidative effect preventing cytokine storm induced by the SARS-CoV-2. Evaluation of the hypothesis: Hemarina is based on the properties of the hemoglobin of the Arenicola marina sea-worm (HEMO2Life®). This extracellular hemoglobin has an oxygen capacity 40 times greater than the hemoglobin of vertebrates. Furthermore, the size of this molecule is 250 times smaller than a human red blood cell, allowing it to diffuse in all areas of the microcirculation, without diffusing outside the vascular sector. It possesses an antioxidative property du a Superoxide Dismutase Activity. This technology has been the subject of numerous publications and HEMO2Life® was found to be well-tolerated and did not induce toxicity. It was administered intravenously to hamsters and rats, and showed no acute effect on heart rate and blood pressure and did not cause microvascular vasoconstriction. In preclinical in vivo models (mice, rats, and dogs), HEMO2Life® has enabled better tissue oxygenation, especially in the brain. This molecule has already been used in humans in organ preservation solutions and the patients showed no abnormal clinical signs. CONSEQUENCES OF THE HYPOTHESIS: The expected benefits of HEMO2Life® for COVID-19 patients are improved survival, avoidance of tracheal intubation, shorter oxygen supplementation, and the possibility of treating a larger number of patients as molecular respirator without to use an invasive machine.


Subject(s)
COVID-19/complications , COVID-19/therapy , Hemoglobins/therapeutic use , Hypoxia/etiology , Hypoxia/therapy , Models, Biological , Oxygen/administration & dosage , Animals , COVID-19/physiopathology , Cricetinae , Dogs , Hemoglobins/administration & dosage , Hemoglobins/metabolism , Humans , Hypoxia/physiopathology , Injections, Intravenous , Mice , Oxidative Stress/drug effects , Oxygen/metabolism , Pandemics , Rats , SARS-CoV-2
9.
Med Hypotheses ; 146: 110411, 2021 01.
Article in English | MEDLINE | ID: covidwho-1225344

ABSTRACT

Many countries across the globe utilized medical and non-medical facemasks as non-pharmaceutical intervention for reducing the transmission and infectivity of coronavirus disease-2019 (COVID-19). Although, scientific evidence supporting facemasks' efficacy is lacking, adverse physiological, psychological and health effects are established. Is has been hypothesized that facemasks have compromised safety and efficacy profile and should be avoided from use. The current article comprehensively summarizes scientific evidences with respect to wearing facemasks in the COVID-19 era, providing prosper information for public health and decisions making.


Subject(s)
COVID-19/prevention & control , Masks , Models, Biological , Pandemics/prevention & control , SARS-CoV-2 , COVID-19/transmission , COVID-19/virology , Humans , Hypercapnia/etiology , Hypercapnia/physiopathology , Hypercapnia/psychology , Hypoxia/etiology , Hypoxia/physiopathology , Hypoxia/psychology , Masks/adverse effects , Masks/standards , Masks/virology , N95 Respirators/adverse effects , N95 Respirators/standards , N95 Respirators/virology , Respiration , Safety , Treatment Outcome
10.
Am J Emerg Med ; 48: 261-268, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1213001

ABSTRACT

BACKGROUND: Emergency Departments (EDs) have served as critical surveillance sites for infectious diseases. We sought to determine the prevalence and temporal trends of acute (by PCR) and convalescent (by antibody [Ab]) SARS-CoV-2 infection during the earliest phase of the pandemic among patients in an urban ED in Baltimore City. METHODS: We tested remnant blood samples from 3255 unique ED patients, collected between March 16th and May 31st 2020 for SARS-CoV-2 Ab. PCR for acute SARS-CoV-2 infection from nasopharyngeal swabs was obtained on any patients based on clinical suspicion. Hospital records were abstracted and factors associated with SARS-CoV-2 infection were assessed. RESULTS: Of 3255 ED patients, 8.2% (95%CI: 7.3%, 9.2%) individuals had evidence of SARS-CoV-2 infection; 155 PCR+, 78 Ab+, and 35 who were both PCR+ and Ab+. Prevalence of disease increased throughout the study period, ranging from 3.2% (95%CI: 1.8%, 5.2%) PCR+ and 0.6% (95%CI: 0.1%, 1.8%) Ab+ in March, to 6.2% (95%CI: 5.1%, 7.4%) PCR+ and 4.2% (95%CI: 3.3%, 5.3%) Ab+ in May. The highest SARS-CoV-2 prevalence was found in Hispanic individuals who made up 8.4% (95%CI: 7.4%, 9.4%) of individuals screened, but 35% (95%CI: 29%, 41%) of infections (PCR and/or Ab+). Demographic and clinical factors independently associated with acute infection included Hispanic ethnicity, loss of smell or taste, subjective fever, cough, muscle ache and fever. Factors independently associated with convalescent infection were Hispanic ethnicity and low oxygen saturation. CONCLUSIONS: The burden of COVID-19 in Baltimore City increased dramatically over the 11-week study period and was disproportionately higher among Hispanic individuals. ED-based surveillance methods are important for identifying both acute and convalescent SARS-CoV-2 infections and provides important information regarding demographic and clinical correlates of disease in the local community.


Subject(s)
COVID-19 Nucleic Acid Testing , COVID-19 Serological Testing , COVID-19/epidemiology , Emergency Service, Hospital , Hypoxia/physiopathology , Acute Disease , Adolescent , Adult , African Americans , Aged , COVID-19/ethnology , COVID-19/physiopathology , Convalescence , Female , Humans , Male , Middle Aged , Prevalence , SARS-CoV-2 , Seroepidemiologic Studies , United States/epidemiology , Young Adult
11.
BMC Pulm Med ; 21(1): 126, 2021 Apr 19.
Article in English | MEDLINE | ID: covidwho-1191325

ABSTRACT

BACKGROUND: Platypnea-orthodeoxia syndrome (POS) is a rare condition characterized by dyspnoea (platypnea) and arterial desaturation in the upright position resolved in the supine position (orthodeoxia). Intracardiac shunt, pulmonary ventilation-perfusion mismatch and others intrapulmonary abnormalities are involved. CASE PRESENTATION: We report a case of POS associated with two pathophysiological issues: one, cardiac POS caused by a patent foramen ovale (PFO) and second, pulmonary POS due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) interstitial pneumonia. POS has resolved after recovery of coronavirus disease 2019 (COVID-19) pneumonia. CONCLUSIONS: Right-to-left interatrial shunt and intrapulmonary shunt caused by SARS-CoV-2 pneumonia contributed to refractory hypoxemia and POS. Therefore, in case of COVID-19 patient with unexplained POS, the existence of PFO must be investigated.


Subject(s)
COVID-19 , Dyspnea , Foramen Ovale, Patent , Hypoxia , Lung/diagnostic imaging , Pneumonia, Viral , COVID-19/diagnosis , COVID-19/physiopathology , Dyspnea/diagnosis , Dyspnea/etiology , Dyspnea/physiopathology , Echocardiography/methods , Foramen Ovale, Patent/complications , Foramen Ovale, Patent/diagnosis , Foramen Ovale, Patent/physiopathology , Hemodynamics , Humans , Hypoxia/diagnosis , Hypoxia/etiology , Hypoxia/physiopathology , Lung Diseases, Interstitial/complications , Lung Diseases, Interstitial/physiopathology , Lung Diseases, Interstitial/virology , Male , Middle Aged , Oxygen/analysis , Pneumonia, Viral/complications , Pneumonia, Viral/diagnosis , Pneumonia, Viral/physiopathology , Posture/physiology , SARS-CoV-2/isolation & purification , Syndrome , Treatment Outcome
13.
Auton Neurosci ; 233: 102810, 2021 07.
Article in English | MEDLINE | ID: covidwho-1188308

ABSTRACT

We have considered some of the available evidence to account for the impact of SARS-CoV on the regulatory control of the autonomic nervous and respiratory systems. Apart from stimulating general interest in the subject, our hope was to provide putative explanations for some of the patients' symptoms based on described physiological and pathophysiological mechanisms seen in other diseases. Herein, we have focused on the carotid bodies. In this hypothetical viewpoint, we have discussed the plasticity of the carotid body chemoreflex and made a comparison between acute and chronic exposures to high altitude with COVID-19. From these discussions, we have postulated that the sensitivity of the hypoxic ventilatory response may well determine the outcome of disease severity and those that live at high altitude may be more resistant. We have provided insight into silent hypoxia and attempted to explain an absence of ventilatory drive and anxiety yet maintenance of consciousness. In an attempt to discover more about the mysteries of COVID-19, we conclude with questions and some hypothetical studies that may answer them.


Subject(s)
Autonomic Nervous System/physiopathology , COVID-19/physiopathology , Carotid Body/physiopathology , Altitude , Carbon Dioxide/metabolism , Cerebrovascular Circulation , Humans , Hypoxia/physiopathology
15.
BMC Pulm Med ; 21(1): 96, 2021 Mar 20.
Article in English | MEDLINE | ID: covidwho-1143203

ABSTRACT

BACKGROUND: Gender-related factors might affect vulnerability to Covid-19. The aim of this study was to describe the role of gender on clinical features and 28-day mortality in Covid-19 patients. METHODS: Observational study of Covid-19 patients hospitalized in Bergamo, Italy, during the first three weeks of the outbreak. Medical records, clinical, radiological and laboratory findings upon admission and treatment have been collected. Primary outcome was 28-day mortality since hospitalization. RESULTS: 431 consecutive adult patients were admitted. Female patients were 119 (27.6%) with a mean age of 67.0 ± 14.5 years (vs 67.8 ± 12.5 for males, p = 0.54). Previous history of myocardial infarction, vasculopathy and former smoking habits were more common for males. At the time of admission PaO2/FiO2 was similar between men and women (228 [IQR, 134-273] vs 238 mmHg [150-281], p = 0.28). Continuous Positive Airway Pressure (CPAP) assistance was needed in the first 24 h more frequently in male patients (25.7% vs 13.0%; p = 0.006). Overall 28-day mortality was 26.1% in women and 38.1% in men (p = 0.018). Gender did not result an independent predictor of death once the parameters related to disease severity at presentation were included in the multivariable analysis (p = 0.898). Accordingly, the Kaplan-Meier survival analysis in female and male patients requiring CPAP or non-invasive ventilation in the first 24 h did not find a significant difference (p = 0.687). CONCLUSION: Hospitalized women are less likely to die from Covid-19; however, once severe disease occurs, the risk of dying is similar to men. Further studies are needed to better investigate the role of gender in clinical course and outcome of Covid-19.


Subject(s)
COVID-19/epidemiology , Aged , Aged, 80 and over , COVID-19/mortality , COVID-19/physiopathology , COVID-19/therapy , Comorbidity , Continuous Positive Airway Pressure/statistics & numerical data , Diabetes Mellitus/epidemiology , Female , Humans , Hypertension/epidemiology , Hypoxia/epidemiology , Hypoxia/physiopathology , Hypoxia/therapy , Italy/epidemiology , Kaplan-Meier Estimate , Male , Middle Aged , Myocardial Infarction/epidemiology , Noninvasive Ventilation/statistics & numerical data , SARS-CoV-2 , Severity of Illness Index , Sex Factors , Smoking/epidemiology
16.
J Appl Physiol (1985) ; 129(6): 1413-1421, 2020 12 01.
Article in English | MEDLINE | ID: covidwho-1064196

ABSTRACT

The transport of oxygen between blood and tissue is limited by blood's capillary transit time, understood as the time available for diffusion exchange before blood returns to the heart. If all capillaries contribute equally to tissue oxygenation at all times, this physical limitation would render vasodilation and increased blood flow insufficient means to meet increased metabolic demands in the heart, muscle, and other organs. In 1920, Danish physiologist August Krogh was awarded the Nobel Prize in Physiology or Medicine for his mathematical and quantitative, experimental demonstration of a solution to this conceptual problem: capillary recruitment, the active opening of previously closed capillaries to meet metabolic demands. Today, capillary recruitment is still mentioned in textbooks. When we suspect symptoms might represent hypoxia of a vascular origin, however, we search for relevant, flow-limiting conditions in our patients and rarely ascribe hypoxia or hypoxemia to short capillary transit times. This review describes how natural changes in capillary transit-time heterogeneity (CTH) and capillary hematocrit (HCT) across open capillaries during blood flow increases can account for a match of oxygen availability to metabolic demands in normal tissue. CTH and HCT depend on a number of factors: on blood properties, including plasma viscosity, the number, size, and deformability of blood cells, and blood cell interactions with capillary endothelium; on anatomical factors including glycocalyx, endothelial cells, basement membrane, and pericytes that affect the capillary diameter; and on any external compression. The review describes how risk factor- and disease-related changes in CTH and HCT interfere with flow-metabolism coupling and tissue oxygenation and discusses whether such capillary dysfunction contributes to vascular disease pathology.


Subject(s)
Capillaries/physiology , Microcirculation , Models, Cardiovascular , Oxygen Consumption , Oxygen/blood , Alzheimer Disease/blood , Alzheimer Disease/physiopathology , Anemia, Sickle Cell/blood , Anemia, Sickle Cell/physiopathology , Animals , Blood Flow Velocity , Cardiovascular Diseases/blood , Cardiovascular Diseases/physiopathology , Diffusion , Humans , Hypoxia/blood , Hypoxia/physiopathology , Regional Blood Flow , Time Factors
18.
Comp Biochem Physiol A Mol Integr Physiol ; 253: 110849, 2021 03.
Article in English | MEDLINE | ID: covidwho-1116507

ABSTRACT

Sequential diving by wild marine mammals results in a lifetime of rapid physiological transitions between lung collapse-reinflation, bradycardia-tachycardia, vasoconstriction-vasodilation, and oxygen store depletion-restoration. The result is a cycle of normoxia and hypoxia in which blood oxygen partial pressures can decline to <20-30 mmHg during a dive, a level considered injurious to oxygen-dependent human tissues (i.e., brain, heart). Safeguards in the form of enhanced on-board oxygen stores, selective oxygen transport, and unique tissue buffering capacities enable marine-adapted mammals to maintain physiological homeostasis and energy metabolism even when breathing and pulmonary gas exchange cease. This stands in stark contrast to the vulnerability of oxygen-sensitive tissues in humans that may undergo irreversible damage within minutes of ischemia and tissue hypoxia. Recently, these differences in protection against hypoxic injury have become evident in the systemic, multi-organ physiological failure during COVID-19 infection in humans. Prolonged recoveries in some patients have led to delays in the return to normal exercise levels and cognitive function even months later. Rather than a single solution to this problem, we find that marine mammals rely on a unique, integrative assemblage of protections to avoid the deleterious impacts of hypoxia on tissues. Built across evolutionary time, these solutions provide a natural template for identifying the potential for tissue damage when oxygen is lacking, and for guiding management decisions to support oxygen-deprived tissues in other mammalian species, including humans, challenged by hypoxia.


Subject(s)
Adaptation, Physiological/physiology , COVID-19/physiopathology , Diving/physiology , Hypoxia/physiopathology , Mammals/physiology , Oxygen/metabolism , Respiration , Animals , COVID-19/metabolism , COVID-19/virology , Humans , Hypoxia/metabolism , Mammals/classification , Mammals/metabolism , SARS-CoV-2/physiology
19.
Rev Alerg Mex ; 67(4): 350-369, 2020.
Article in Spanish | MEDLINE | ID: covidwho-1106728

ABSTRACT

Coronavirus disease 2019 (COVID-19) is an infection caused by SARS-CoV-2 that has caused an unprecedented pandemic with a high rate of morbidity and mortality worldwide. Although most cases are mild, there are a considerable number of patients who develop pneumonia or even acute respiratory distress syndrome (ARDS). After having recovered from the initial disease, many patients continue with various symptoms (fatigue, dry cough, fever, dyspnea, anosmia, and chest pain, among others.), which has led to consider the possible existence of "post-COVID-19 syndrome". Although the definition and validity of this syndrome are not clear yet, several studies report that individuals who have recovered from COVID-19 may have persistent symptoms, radiological abnormalities, and compromised respiratory function. Current evidence suggests that there is a large number of pulmonary sequelae after COVID-19 pneumonia (interstitial thickening, ground glass opacities, crazy paving pattern, and bronchiectasis, among others.). Likewise, it seems that pulmonary function tests (spirometry, DLCO, 6MWT, and measurement of maximum respiratory pressures), in addition to high-resolution computed axial tomographies (CAT scan), are useful for the assessment of these post-COVID-19 pulmonary sequelae. This review aims to describe the possible pulmonary sequelae after COVID-19 pneumonia, as well as to suggest diagnostic procedures for their correct assessment and follow-up; thus, allowing proper management by a multidisciplinary medical team.


COVID-19 es la enfermedad causada por el virus SARS-CoV-2, la cual ha ocasionado una pandemia sin precedentes, con gran cantidad de infectados y muertos en el mundo. Aunque la mayoría de los casos son leves, existe una cantidad considerable de pacientes que desarrollan neumonía o, incluso, síndrome de distrés respiratorio agudo (SDRA). Luego de recuperarse del cuadro inicial, muchos pacientes continúan con diversos síntomas (fatiga, tos seca, fiebre, disnea, anosmia, dolor torácico, entre otras), lo que ha llevado a considerar la posible existencia del "síndrome pos-COVID-19". Aunque la definición y validez de este síndrome aún no son claras, varios estudios reportan que los individuos recuperados de la COVID-19 pueden tener persistencia de síntomas, anormalidades radiológicas y compromiso en la función respiratoria. La evidencia actual sugiere que existe gran cantidad de secuelas pulmonares despues de una neumonía por COVID-19 (engrosamiento intersticial, infiltrado en vidrio esmerilado, patrón en empedrado, bronquiectasias, entre otras.). De igual forma, parece ser que las pruebas de función pulmonar (espirometría, prueba de difusión pulmonar de monóxido de carbono, prueba de caminata de seis minutos y la medición de las presiones respiratorias máximas), además de la tomografía axial computarizada de alta resolución, son útiles para evaluar las secuelas pulmonares pos-COVID-19. En esta revisión se pretende describir las posibles secuelas a nivel pulmonar posteriores a neumonía por COVID-19, así como sugerir procedimientos diagnósticos para su correcta evaluación y seguimiento, que permitan el manejo adecuado por parte de un equipo médico multidisciplinario.


Subject(s)
COVID-19/complications , Convalescence , Lung Diseases/etiology , Respiratory Distress Syndrome/etiology , Bronchiectasis/diagnostic imaging , Bronchiectasis/etiology , Bronchiectasis/physiopathology , Disease Progression , Follow-Up Studies , Humans , Hypoxia/blood , Hypoxia/etiology , Hypoxia/physiopathology , Lung Diseases/diagnostic imaging , Lung Diseases, Interstitial/diagnostic imaging , Lung Diseases, Interstitial/etiology , Lung Diseases, Interstitial/physiopathology , Mental Disorders/etiology , Mental Disorders/physiopathology , Oxygen/blood , Pulmonary Embolism/diagnostic imaging , Pulmonary Embolism/etiology , Pulmonary Embolism/physiopathology , Respiratory Distress Syndrome/physiopathology , Respiratory Function Tests , Spirometry , Tomography, X-Ray Computed
20.
Pediatr Pulmonol ; 55(1): 229-235, 2020 01.
Article in English | MEDLINE | ID: covidwho-1064409

ABSTRACT

BACKGROUND: In utero diaphragm development is critically important for postnatal respiratory function and any disturbance to fetal development may lead to diaphragm dysfunction and respiratory complications in the postnatal period. Intrauterine growth restriction (IUGR) has been shown to affect respiratory function in a sex-dependent manner; however, the effect of IUGR on diaphragm function is unknown. AIM: This study used a maternal hypoxia-induced mouse model of IUGR to investigate the impact of IUGR on diaphragm function and structure in male and female adult offspring. MATERIALS AND METHODS: Pregnant BALB/c mice were housed under hypoxic conditions (10.5% O2 ) from gestational days 11 to 17.5 and then returned to normoxic conditions. Control mice were housed under normoxic conditions throughout pregnancy. At 8 weeks of age, offspring were euthanized and diaphragms isolated for functional assessment in organ bath experiments and for histological analysis. RESULTS: IUGR offspring were lighter at birth and remained lighter at 8 weeks of age compared to Controls. While diaphragm force (maximal or twitch) was not affected by treatment or sex, the IUGR group exhibited a longer half-relaxation time after twitch contractions compared to Control. Female offspring had a lower maximum rate of force development and higher fatigue resistance compared to males, independent of IUGR. There was no difference in the diaphragm myofibre cross-sectional area between groups or sexes. CONCLUSION: Sex and IUGR independently affect diaphragm contraction in adult mice without changes in structure. This study demonstrates that IUGR affects diaphragm contractile function in later life and could impair respiratory function if exacerbated under conditions of increased respiratory load.


Subject(s)
Diaphragm/physiopathology , Fetal Growth Retardation/physiopathology , Animals , Disease Models, Animal , Female , Fetal Growth Retardation/etiology , Hypoxia/complications , Hypoxia/physiopathology , Male , Mice , Mice, Inbred BALB C , Pregnancy
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