Sevoflurane, Compared With Isoflurane, Minimizes Lung Damage in Pulmonary but Not in Extrapulmonary Acute Respiratory Distress Syndrome in Rats

COVID-19, a disease caused by the novel coronavirus SARS-CoV-2, primarily affects lung tissue and disrupts gas exchange, leading to acute respiratory distress syndrome, systemic hypoxia, and lung damage. The search for methods of prevention and rehabilitation, especially after suffering from pneumonia caused by COVID-19, is on the agenda. This article discusses the possibilities of the interval hypoxic training (IHT) method for preventing infections by initiating nitric oxide production in the body. One of the main effects of IHT is the balanced stimulation of nitric oxide (NO) secretion. Over the past two decades, there has been an increasing interest in the function of nitric oxide (NO) in the human body. Nitric oxide plays a key role in maintaining normal vascular function and regulating inflammatory processes, including those leading to lung damage and the development of acute respiratory distress syndrome (ARDS). Our immune system destroys bacteria and viruses by oxidative burst, i.e. when oxygen accumulates inside the cell. This process also involves nitric oxide, a signaling molecule that has an antibacterial and antiviral effect, as well as regulates vascular tone and affects the permeability of the cell wall. Interval hypoxytherapy enhances endogenous oxidative protection and increases the amount of nitric oxide, thus allowing the body’s cells to resist infection more effectively. Mitochondrial NOS induction and mitochondrial NO synthesis increase under the action of pathogenic factors on the cell. By modulating the activity of mtNOS and the synthesis of mitochondrial NO, it is possible to increase the resistance to hypoxic effects. Interval hypo-hyperoxic training as an effective non-specific method of increasing the body’s defenses is indispensable not only in the prevention of viral infection, but also in rehabilitation after viral pneumonia, as well as as a method that reduces the severity of viral infection in the event of infection.

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Protective - ventilation strategy in the acute respiratory distress syndrome

Acta chirurgica iugoslavica ◽

10.2298/aci0403045b ◽

2004 ◽

Vol 51 (3) ◽

pp. 45-49 ◽

Cited By ~ 1

Author(s):

Vladimir Bumbasirevic ◽

V. Bukumirovic ◽

Nada Popovic ◽

V. Nikolic ◽

Nevena Kalezic ◽

...

Keyword(s):

Mechanical Ventilation ◽

Acute Respiratory Distress Syndrome ◽

Lung Injury ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Pulmonary Ventilation ◽

Lung Damage ◽

Ventilatory Strategy ◽

Protective Ventilation Strategy

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) contribute to progressive hypoxemia in critically ill patients. It has been proved that conventional mechanical ventilation with physiological respiratory volume contributes to further lung damage. In this respect, application of protective ventilatory strategy - pulmonary ventilation with limited volume and pressure can avoid mentioned consequences. The aim of this paper is to discuss mechanims by which elements contained in protective mechanical ventilation of patients with ALI/ARDS prevent further progrssive lung injury, to argue the effects of positive end - expiratory pressure and present insturctions for its application.

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Impact of Ventilator-Subject Asynchrony on the Work of Breathing and Lung Damage in Experimental Acute Respiratory Distress Syndrome

10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1136 ◽

2019 ◽

Author(s):

J.J.M. Wittenstein ◽

M. Scharffenberg ◽

R. Huhle ◽

T. Bluth ◽

M. Leidermann ◽

...

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Work Of Breathing ◽

Lung Damage

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Recovery of COVID-19 acute respiratory distress syndrome with tocilizumab: successful outcome in two critically ill patients

Immunotherapy ◽

10.2217/imt-2020-0154 ◽

2020 ◽

Vol 12 (15) ◽

pp. 1127-1132 ◽

Cited By ~ 4

Author(s):

Juan David Cala-García ◽

Juan David Sierra-Bretón ◽

Jorge Eduardo Cavelier-Baiz ◽

Álvaro A Faccini-Martínez ◽

Carlos Eduardo Pérez-Díaz

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Severe Pneumonia ◽

Lung Damage ◽

Successful Outcome ◽

Cytokine Storm ◽

Principal Mechanism ◽

Prior Administration

Background: Severe pneumonia and acute respiratory distress syndrome (ARDS) due to COVID-19 is a challenge for nowadays medical practice. Although there is no clarity in the principal mechanism of lung damage and ARDS development, it has been suggested that one of the main reasons of this pathology is the hyperactivation of the immune system, better known as cytokine storm syndrome. Tocilizumab has been proposed to treat COVID-19 severe cases associated to ARDS. Results & methodology: Here we present two successful cases of tocilizumab administration in two COVID-19 patients with prior administration of antiviral therapy (hydroxychloroquine, azithromycin, lopinavir and ritonavir) with adequate response and resolution of ARDS, septic shock and severe pneumonia within the first 72 h. Discussion & conclusion: This case supports the usage of tocilizumab as an effective therapy in COVID-19 associated cytokine storm syndrome. Further studies should be done in order to assess its effectiveness and security.

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Clinical characteristics and prognosis of drug-associated acute respiratory distress syndrome compared with non-drug-associated acute respiratory distress syndrome: a single-centre retrospective study in Japan

BMJ Open ◽

10.1136/bmjopen-2016-015330 ◽

2017 ◽

Vol 7 (11) ◽

pp. e015330 ◽

Cited By ~ 4

Author(s):

Keisuke Anan ◽

Kazuya Ichikado ◽

Kodai Kawamura ◽

Takeshi Johkoh ◽

Kiminori Fujimoto ◽

...

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Arterial Oxygen Tension ◽

Ventilator Weaning ◽

Serum Lactate ◽

Lung Damage ◽

Arterial Oxygen ◽

Serum Lactate Dehydrogenase

ObjectivesTo report the clinical features and prognosis of drug-associatedacute respiratory distress syndrome (ARDS).DesignA retrospective analysis of data collected during a prospective cohort study.SettingIntensive care unit in a teaching hospital.ParticipantsA total of 197 Japanese patients with ARDS diagnosed by the Berlin definition who were admitted to the Division of Respiratory Medicine from October 2004 to December 2015 were enrolled in the study and were classified as two groups according to their causes: a drug-associated ARDS group (n=27) and a non-drug-associated ARDS group (n=170). Primary outcome measure is 28-day mortality, and the secondaryoutcome measure is ventilator-free days.ResultsThe Acute Physiology and Chronic Health Evaluation II scores were significantly lower in the drug-associated ARDS group than in the non-drug-associated ARDS group (median (IQR): 18.0 (16.5–21.0) vs 23.0 (18.0–26.0), p<0.001), and the arterial oxygen tension/fractional inspired oxygen ratio was higher (148.0 (114.1–177.5) vs 101.0 (71.5–134.0), p=0.003). In the drug-associated ARDS group, although high-resolution CT scores indicative of the extent of fibroproliferation (301.6 (244.1–339.8) vs 208.3 (183.4–271.6), p<0.001), serum lactate dehydrogenase levels (477 (365–585) vs 322 (246–434), p=0.003) and the McCabe scores (score 1/2/3, n (%): 20 (74)/4 (15)/3 (11)vs154 (91)/7 (4)/9 (5), p=0.04) were significantly higher, ventilator weaning was earlier (p<0.001) and 28-day mortality was better (p=0.043). After adjusting for potentially confounding covariates, drug-associated ARDS group was associated with lower 28-day mortality (adjusted HR (HR) 0.275; 95% CI 0.106 to 0.711; p=0.008).ConclusionsAlthough more severe lung damage with fibroproliferation was observed in patients with drug-associated ARDS, ventilator weaning was earlier, and their prognosis was better than the others. Further well-designed prospective studies are needed.

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Recent insights: mesenchymal stromal/stem cell therapy for acute respiratory distress syndrome

F1000Research ◽

10.12688/f1000research.8217.1 ◽

2016 ◽

Vol 5 ◽

pp. 1532 ◽

Cited By ~ 12

Author(s):

Shahd Horie ◽

John G. Laffey

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Therapeutic Option ◽

Ischemia Reperfusion ◽

Scale Up ◽

Cell Interaction ◽

Lung Damage

Acute respiratory distress syndrome (ARDS) causes respiratory failure, which is associated with severe inflammation and lung damage and has a high mortality and for which there is no therapy. Mesenchymal stromal/stem cells (MSCs) are adult multi-progenitor cells that can modulate the immune response and enhance repair of damaged tissue and thus may provide a therapeutic option for ARDS. MSCs demonstrate efficacy in diverse in vivo models of ARDS, decreasing bacterial pneumonia and ischemia-reperfusion-induced injury while enhancing repair following ventilator-induced lung injury. MSCs reduce the pro-inflammatory response to injury while augmenting the host response to bacterial infection. MSCs appear to exert their effects via multiple mechanisms—some are cell interaction dependent whereas others are paracrine dependent resulting from both soluble secreted products and microvesicles/exosomes derived from the cells. Strategies to further enhance the efficacy of MSCs, such as by overexpressing anti-inflammatory or pro-repair molecules, are also being investigated. Encouragingly, early phase clinical trials of MSCs in patients with ARDS are under way, and experience with these cells in trials for other diseases suggests that the cells are well tolerated. Although considerable translational challenges, such as concerns regarding cell manufacture scale-up and issues regarding cell potency and batch variability, must be overcome, MSCs constitute a highly promising potential therapy for ARDS.

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Countermeasure and therapeutic: A(1–7) to treat acute respiratory distress syndrome due to COVID-19 infection

Journal of the Renin-Angiotensin-Aldosterone System ◽

10.1177/1470320320972018 ◽

2020 ◽

Vol 21 (4) ◽

pp. 147032032097201

Author(s):

Maira Soto ◽

Gere diZerega ◽

Kathleen E Rodgers

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Oxidative Damage ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Renin Angiotensin System ◽

Lung Damage ◽

Novel Therapies ◽

Angiotensin System ◽

Models Of Disease

In the wake of the COVID-19 pandemic it has become clear that there is a need for therapies that are capable of reducing damage caused to patients from infections. Infections that induce Acute Respiratory Distress Syndrome (ARDS) are especially devastating because lung damage is so critical and difficult to manage. Angiotensin (1–7) [A(1–7)] has already been shown to protect pulmonary health and architecture in various models of disease. There is also evidence that A(1–7) can modulate immune function and protect various organs (lung, kidney, and heart) from oxidative damage and inflammation. Here we focus on making a case for the development of novel therapies that target the protective arm of the Renin Angiotensin System (RAS).

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Definitions, Epidemiology, Clinical Risk Factors, and Health Disparities in Acute Respiratory Distress Syndrome

Seminars in Respiratory and Critical Care Medicine ◽

10.1055/s-0039-1683884 ◽

2019 ◽

Vol 40 (01) ◽

pp. 003-011 ◽

Cited By ~ 1

Author(s):

Mohleen Kang ◽

Jordan Kempker

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Temporal Trends ◽

Epidemiologic Study ◽

Case Fatality ◽

Rapid Onset ◽

Case Definition ◽

Lung Damage

AbstractAcute respiratory distress syndrome (ARDS) is a syndrome of inflammatory lung injury currently defined as the rapid onset of hypoxemia and radiographic opacities from a recent direct or indirect insult that is not explained by other causes. While the diagnostic criteria used to define ARDS are helpful in the clinical setting, they are not entirely specific for the characteristic pathophysiology of diffuse alveolar lung damage. This case definition introduces challenges to the reliable and accurate epidemiologic study of the condition. Within these limitations, ARDS appears to be a condition that is relatively rare within the general population but common within the context of the intensive care unit. Furthermore, the frequency and outcomes of ARDS seem to vary between populations, with no clearly discernible temporal trends in incidence or case fatality that are uniform across studies.

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Gradually Increasing Tidal Volume May Mitigate Experimental Lung Injury in Rats

Anesthesiology ◽

10.1097/aln.0000000000002630 ◽

2019 ◽

Vol 130 (5) ◽

pp. 767-777 ◽

Cited By ~ 6

Author(s):

Nathane S. Felix ◽

Cynthia S. Samary ◽

Fernanda F. Cruz ◽

Nazareth N. Rocha ◽

Marcos V. S. Fernandes ◽

...

Keyword(s):

Extracellular Matrix ◽

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Tidal Volume ◽

Distress Syndrome ◽

Alveolar Epithelial Cells ◽

Lung Damage ◽

Adaptation Period ◽

Adaptation Time

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background This study hypothesized that, in experimental mild acute respiratory distress syndrome, lung damage caused by high tidal volume (VT) could be attenuated if VT increased slowly enough to progressively reduce mechanical heterogeneity and to allow the epithelial and endothelial cells, as well as the extracellular matrix of the lung to adapt. For this purpose, different strategies of approaching maximal VT were tested. Methods Sixty-four Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 h, animals were randomly assigned to receive mechanical ventilation with VT = 6 ml/kg for 2 h (control); VT = 6 ml/kg during hour 1 followed by an abrupt increase to VT = 22 ml/kg during hour 2 (no adaptation time); VT = 6 ml/kg during the first 30 min followed by a gradual VT increase up to 22 ml/kg for 30 min, then constant VT = 22 ml/kg during hour 2 (shorter adaptation time); and a more gradual VT increase, from 6 to 22 ml/kg during hour 1 followed by VT = 22 ml/kg during hour 2 (longer adaptation time). All animals were ventilated with positive end-expiratory pressure of 3 cm H2O. Nonventilated animals were used for molecular biology analysis. Results At 2 h, diffuse alveolar damage score and heterogeneity index were greater in the longer adaptation time group than in the control and shorter adaptation time animals. Gene expression of interleukin-6 favored the shorter (median [interquartile range], 12.4 [9.1–17.8]) adaptation time compared with longer (76.7 [20.8 to 95.4]; P = 0.02) and no adaptation (65.5 [18.1 to 129.4]) time (P = 0.02) strategies. Amphiregulin, metalloproteinase-9, club cell secretory protein-16, and syndecan showed similar behavior. Conclusions In experimental mild acute respiratory distress syndrome, lung damage in the shorter adaptation time group compared with the no adaptation time group was attenuated in a time-dependent fashion by preemptive adaptation of the alveolar epithelial cells and extracellular matrix. Extending the adaptation period increased cumulative power and did not prevent lung damage, because it may have exposed animals to injurious strain earlier and for a longer time, thereby negating any adaptive benefit.

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Loratadine syrup is successfully used to fix Covid-19 induced respiratory distress and chest pain

Journal of Clinical Images and Medical Case Reports ◽

10.52768/2766-7820/1424 ◽

2021 ◽

Vol 2 (6) ◽

Author(s):

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Chest Pain ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Viral Infection ◽

Distress Syndrome ◽

Pregnant Patient ◽

Lung Damage

COVID-19 disease is a highly transmissible viral infection caused by the SARS-CoV-2 coronavirus. This virus can cause lung damage, acute respiratory distress syndrome and death. In this case, How Covid-19 in a pregnant patient which didn’t respond well to Vancomyci + Caftazidime + Dexamethasone + Heparin for 7 days was finally responded to Loratadine syrup, and the patient was cured is going to be presented.

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