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  1. Article ; Online: Two years of the COVID-19 pandemic: an anesthesiology perspective.

    Schmidt, André P / Módolo, Norma S P / de Amorim, Célio G / Simões, Cláudia M / Kraychete, Durval C / Joaquim, Eduardo H G / Lineburger, Eric B / Papa, Fábio V / Fernandes, Fátima C / Mendes, Florentino F / Guimarães, Gabriel M N / Barros, Guilherme A M / Silva-Jr, João M / Navarro E Lima, Laís H / Azi, Liana M T A / Carvalho, Lorena I M / Stefani, Luciana C / Garcia, Luis V / Malbouisson, Luiz Marcelo S /
    Salgado-Filho, Marcello F / Nascimento Junior, Paulo do / Alves, Rodrigo L / Carvalho, Vanessa H / Quintão, Vinicius C / Carmona, Maria José C

    Brazilian journal of anesthesiology (Elsevier)

    2022  Volume 72, Issue 2, Page(s) 165–168

    MeSH term(s) Anesthesiology ; COVID-19 ; Humans ; Pandemics ; SARS-CoV-2
    Language English
    Publishing date 2022-02-19
    Publishing country Brazil
    Document type Editorial
    ZDB-ID 1142792-9
    ISSN 0104-0014 ; 0104-0014
    ISSN (online) 0104-0014
    ISSN 0104-0014
    DOI 10.1016/j.bjane.2022.02.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Sevoflurane, Compared With Isoflurane, Minimizes Lung Damage in Pulmonary but Not in Extrapulmonary Acute Respiratory Distress Syndrome in Rats.

    Araújo, Mariana N / Santos, Cíntia L / Samary, Cynthia S / Heil, Luciana B B / Cavalcanti, Vinicius C M / Cruz, Fernanda F / Felix, Nathane S / Silva, Johnatas D / Morales, Marcelo M / Pelosi, Paolo / Fernandes, Fatima C / Villela, Nivaldo R / Silva, Pedro L / Rocco, Patricia R M

    Anesthesia and analgesia

    2017  Volume 125, Issue 2, Page(s) 491–498

    Abstract: Background: Volatile anesthetics modulate inflammation in acute respiratory distress syndrome (ARDS). However, it is unclear whether they act differently depending on ARDS etiology. We hypothesized that the in vivo and in vitro effects of sevoflurane ... ...

    Abstract Background: Volatile anesthetics modulate inflammation in acute respiratory distress syndrome (ARDS). However, it is unclear whether they act differently depending on ARDS etiology. We hypothesized that the in vivo and in vitro effects of sevoflurane and isoflurane on lung damage would not differ in pulmonary (p) and extrapulmonary (exp) ARDS.
    Methods: Twenty-four Wistar rats were randomized to undergo general anesthesia (1-2 minutes) with sevoflurane and isoflurane. Animals were then further randomized to receive Escherichia coli lipopolysaccharide (LPS) intratracheally (ARDSp) or intraperitoneally (ARDSexp), and 24 hours after ARDS induction, they were subjected to 60 minutes of sevoflurane or isoflurane anesthesia at 1 minimal alveolar concentration. The primary outcome measure was interleukin (IL)-6 mRNA expression in lung tissue. Secondary outcomes included gas exchange, lung mechanics, histology, and mRNA expression of IL-10, nuclear factor erythroid 2-related factor-2 (Nrf2), surfactant protein (SP)-B, vascular cell adhesion molecule-1, epithelial amiloride-sensitive Na-channel subunits α and γ, and sodium-potassium-adenosine-triphosphatase pump subunits α1 (α1-Na,K-ATPase) and β1 (β1-Na,K-ATPase). Additional ARDSp and ARDSexp animals (n = 6 per group) were anesthetized with sodium thiopental but not mechanically ventilated (NV) to serve as controls. Separately, to identify how sevoflurane and isoflurane act on type II epithelial cells, A549 human lung epithelial cells were stimulated with LPS (20 µg/mL) for 24 hours, and SP-B expression was quantified after further exposure to sevoflurane or isoflurane (1 minimal alveolar concentration ) for 60 minutes.
    Results: In ARDSp, sevoflurane reduced IL-6 expression to a greater degree than isoflurane (P = .04). Static lung elastance (P = .0049) and alveolar collapse (P = .033) were lower in sevoflurane than isoflurane, whereas Nrf2 (P = .036), SP-B (P = .042), and β1-Na,K-ATPase (P = .038) expressions were higher in sevoflurane. In ARDSexp, no significant differences were observed in lung mechanics, alveolar collapse, or molecular parameters between sevoflurane and isoflurane. In vitro, SP-B expression was higher in sevoflurane than isoflurane (P = .026).
    Conclusions: Compared with isoflurane, sevoflurane did not affect lung inflammation in ARDSexp, but it did reduce lung inflammation in ARDSp.
    MeSH term(s) A549 Cells ; Anesthetics ; Animals ; Escherichia coli ; Female ; Humans ; Inflammation ; Interleukin-6/metabolism ; Isoflurane/therapeutic use ; Lipopolysaccharides/administration & dosage ; Lung/drug effects ; Methyl Ethers/therapeutic use ; Oxidative Stress ; Random Allocation ; Rats ; Rats, Wistar ; Respiratory Distress Syndrome, Adult/drug therapy ; Respiratory Distress Syndrome, Adult/etiology ; Time Factors
    Chemical Substances Anesthetics ; Interleukin-6 ; Lipopolysaccharides ; Methyl Ethers ; sevoflurane (38LVP0K73A) ; Isoflurane (CYS9AKD70P)
    Language English
    Publishing date 2017-08
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 80032-6
    ISSN 1526-7598 ; 0003-2999
    ISSN (online) 1526-7598
    ISSN 0003-2999
    DOI 10.1213/ANE.0000000000001927
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The Effects of Short-Term Propofol and Dexmedetomidine on Lung Mechanics, Histology, and Biological Markers in Experimental Obesity.

    Heil, Luciana Boavista Barros / Santos, Cíntia L / Santos, Raquel S / Samary, Cynthia S / Cavalcanti, Vinicius C M / Araújo, Mariana M P N / Poggio, Hananda / Maia, Lígia de A / Trevenzoli, Isis Hara / Pelosi, Paolo / Fernandes, Fatima C / Villela, Nivaldo R / Silva, Pedro L / Rocco, Patricia R M

    Anesthesia and analgesia

    2016  Volume 122, Issue 4, Page(s) 1015–1023

    Abstract: Background: Administering anesthetics to the obese population requires caution because of a variety of reasons including possible interactions with the inflammatory process observed in obese patients. Propofol and dexmedetomidine have protective effects ...

    Abstract Background: Administering anesthetics to the obese population requires caution because of a variety of reasons including possible interactions with the inflammatory process observed in obese patients. Propofol and dexmedetomidine have protective effects on pulmonary function and are widely used in short- and long-term sedation, particularly in intensive care unit settings in lean and obese subjects. However, the functional and biological effects of these drugs in obesity require further elucidation. In a model of diet-induced obesity, we compared the short-term effects of dexmedetomidine versus propofol on lung mechanics and histology, as well as biological markers of inflammation and oxidative stress modulation in obesity.
    Methods: Wistar rats (n = 56) were randomly fed a standard diet (lean) or experimental diet (obese) for 12 weeks. After this period, obese animals received sodium thiopental intraperitoneally and were randomly allocated into 4 subgroups: (1) nonventilated (n = 4) for molecular biology analysis only (control); (2) sodium thiopental (n = 8); (3) propofol (n = 8); and (4) dexmedetomidine (n = 8), which received continuous IV administration of the corresponding agents and were mechanically ventilated (tidal volume = 6 mL/kg body weight, fraction of inspired oxygen = 0.4, positive end-expiratory pressure = 3 cm H2O) for 1 hour.
    Results: Compared with lean animals, obese rats did not present increased body weight but had higher total body and trunk fat percentages, airway resistance, and interleukin-6 levels in the lung tissue (P = 0.02, P = 0.0027, and P = 0.01, respectively). In obese rats, propofol, but not dexmedetomidine, yielded increased airway resistance, bronchoconstriction index (P = 0.016, P = 0.02, respectively), tumor necrosis factor-α, and interleukin-6 levels, as well as lower levels of nuclear factor-erythroid 2-related factor-2 and glutathione peroxidase (P = 0.001, Bonferroni-corrected t test).
    Conclusions: In this model of diet-induced obesity, a 1-hour propofol infusion yielded increased airway resistance, atelectasis, and lung inflammation, with depletion of antioxidative enzymes. However, unlike sodium thiopental and propofol, short-term infusion of dexmedetomidine had no impact on lung morphofunctional and biological variables.
    MeSH term(s) Animals ; Biomarkers/metabolism ; Dexmedetomidine/administration & dosage ; Lung/drug effects ; Lung/metabolism ; Lung/pathology ; Male ; Obesity/drug therapy ; Obesity/metabolism ; Obesity/pathology ; Propofol/administration & dosage ; Rats ; Rats, Wistar ; Respiration, Artificial/adverse effects ; Respiratory Mechanics/drug effects ; Respiratory Mechanics/physiology ; Treatment Outcome
    Chemical Substances Biomarkers ; Dexmedetomidine (67VB76HONO) ; Propofol (YI7VU623SF)
    Language English
    Publishing date 2016-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80032-6
    ISSN 1526-7598 ; 0003-2999
    ISSN (online) 1526-7598
    ISSN 0003-2999
    DOI 10.1213/ANE.0000000000001114
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Effects of dexmedetomidine on respiratory mechanics and control of breathing in normal rats.

    Fernandes, Fatima C / Ferreira, Halina C / Cagido, Viviane R / Carvalho, Giovanna M C / Pereira, Leonel S / Faffe, Debora S / Zin, Walter A / Rocco, Patricia R M

    Respiratory physiology & neurobiology

    2006  Volume 154, Issue 3, Page(s) 342–350

    Abstract: Dexmedetomidine is a highly selective and specific alpha(2)-adrenergic agonist, with sedative, analgesic, and sympatholytic activities. The aim of the present study was to define the effects of DMED in respiratory mechanics in normal rats. In addition, ... ...

    Abstract Dexmedetomidine is a highly selective and specific alpha(2)-adrenergic agonist, with sedative, analgesic, and sympatholytic activities. The aim of the present study was to define the effects of DMED in respiratory mechanics in normal rats. In addition, lung morphometry was studied to determine whether the physiological changes reflected underlying morphological changes defining the sites of action of dexmedetomidine. Arterial blood gases were also determined. Twelve adult Wistar rats were randomly assigned to two groups of six animals each: PENTO and DMED. In PENTO group animals were sedated (diazepam, 5mg, i.p.) and anaesthetised with pentobarbital sodium (20mgkg(-1) i.p.). The rats of the DMED group received dexmedetomidine (250mugkg(-1) i.p. followed by intravenous infusion of 0.5mugkg(-1)h(-1)). In spontaneously breathing rats, minute ventilation, respiratory frequency, and neuromuscular inspiratory drive were lower in dexmedetomidine group, which also presented hypercapnia, whereas tidal volume, inspiratory, expiratory, and total respiratory cycle times were higher in dexmedetomidine group compared to the PENTO group. During mechanical ventilation, respiratory mechanical parameters were similar in both groups. These findings were supported by the absence of histological changes. In conclusion, under the conditions studied, dexmedetomidine did not change respiratory mechanical parameters and lung histology, but induced ventilatory depression.
    MeSH term(s) Adrenergic alpha-Agonists/administration & dosage ; Adrenergic alpha-Agonists/pharmacology ; Anesthesia ; Animals ; Dexmedetomidine/administration & dosage ; Dexmedetomidine/pharmacology ; Diazepam/pharmacology ; Hypnotics and Sedatives/administration & dosage ; Hypnotics and Sedatives/pharmacology ; Inhalation/drug effects ; Injections, Intraperitoneal ; Lung/anatomy & histology ; Lung/drug effects ; Male ; Pentobarbital ; Rats ; Rats, Wistar ; Respiration/drug effects ; Respiration, Artificial ; Respiratory Mechanics/drug effects
    Chemical Substances Adrenergic alpha-Agonists ; Hypnotics and Sedatives ; Dexmedetomidine (67VB76HONO) ; Pentobarbital (I4744080IR) ; Diazepam (Q3JTX2Q7TU)
    Language English
    Publishing date 2006-12
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2077867-3
    ISSN 1878-1519 ; 1569-9048
    ISSN (online) 1878-1519
    ISSN 1569-9048
    DOI 10.1016/j.resp.2006.02.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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