Liliane Nardelli

Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil

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Publications (8)19.97 Total impact

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    ABSTRACT: We investigated the effects of acute hypercapnic acidosis and buffered hypercapnia on lung inflammation and apoptosis in experimental acute lung injury (ALI). Twenty-four hours after paraquat injection, 28 Wistar rats were randomized into four groups (n = 7/group): (1) normocapnia (NC, PaCO2 = 35-45 mmHg), ventilated with 0.03%CO2 + 21%O2 + balanced N2; (2) hypercapnic acidosis (HC, PaCO2 = 60-70 mmHg), ventilated with 5%CO2 + 21%O2 + balanced N2; and (3) buffered hypercapnic acidosis (BHC), ventilated with 5%CO2 + 21%O2 + balanced N2 and treated with sodium bicarbonate (8.4%). The remaining seven animals were not mechanically ventilated (NV). The mRNA expression of interleukin (IL)-6 (p = 0.003), IL-1β (p < 0.001), and type III procollagen (PCIII) (p = 0.001) in lung tissue was more reduced in the HC group in comparison with NC, with no significant differences between HC and BHC. Lung and kidney cell apoptosis was reduced in HC and BHC in comparison with NC and NV. In conclusion, in this experimental ALI model, hypercapnia, regardless of acidosis, reduced lung inflammation and lung and kidney cell apoptosis.
    Respiratory Physiology & Neurobiology 09/2014; · 2.05 Impact Factor
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    ABSTRACT: In acute lung injury, recruitment maneuvers have been used to open collapsed lungs and set positive end-expiratory pressure, but their effectiveness may depend on the degree of lung injury. This study uses a single experimental model with different degrees of lung injury and tests the hypothesis that recruitment maneuvers may have beneficial or deleterious effects depending on the severity of acute lung injury. We speculated that recruitment maneuvers may worsen lung mechanical stress in the presence of alveolar edema. Prospective, randomized, controlled experimental study. University research laboratory. Thirty-six Wistar rats randomly divided into three groups (n = 12 per group). In the control group, saline was intraperitoneally injected, whereas moderate and severe acute lung injury animals received paraquat intraperitoneally (20 mg/kg [moderate acute lung injury] and 25 mg/kg [severe acute lung injury]). After 24 hrs, animals were further randomized into subgroups (n = 6/each) to be recruited (recruitment maneuvers: 40 cm H₂O continuous positive airway pressure for 40 secs) or not, followed by 1 hr of protective mechanical ventilation (tidal volume, 6 mL/kg; positive end-expiratory pressure, 5 cm H₂O). Only severe acute lung injury caused alveolar edema. The amounts of alveolar collapse were similar in the acute lung injury groups. Static lung elastance, viscoelastic pressure, hyperinflation, lung, liver, and kidney cell apoptosis, and type 3 procollagen and interleukin-6 mRNA expressions in lung tissue were more elevated in severe acute lung injury than in moderate acute lung injury. After recruitment maneuvers, static lung elastance, viscoelastic pressure, and alveolar collapse were lower in moderate acute lung injury than in severe acute lung injury. Recruitment maneuvers reduced interleukin-6 expression with a minor detachment of the alveolar capillary membrane in moderate acute lung injury. In severe acute lung injury, recruitment maneuvers were associated with hyperinflation, increased apoptosis of lung and kidney, expression of type 3 procollagen, and worsened alveolar capillary injury. In the presence of alveolar edema, regional mechanical heterogeneities, and hyperinflation, recruitment maneuvers promoted a modest but consistent increase in inflammatory and fibrogenic response, which may have worsened lung function and potentiated alveolar and renal epithelial injury.
    Critical care medicine 11/2010; 38(11):2207-14. · 6.37 Impact Factor
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    ABSTRACT: The goal of the study was to compare the effects of different assisted ventilation modes with pressure controlled ventilation (PCV) on lung histology, arterial blood gases, inflammatory and fibrogenic mediators in experimental acute lung injury (ALI). Paraquat-induced ALI rats were studied. At 24 h, animals were anaesthetised and further randomized as follows (n = 6/group): (1) pressure controlled ventilation mode (PCV) with tidal volume (V (T)) = 6 ml/kg and inspiratory to expiratory ratio (I:E) = 1:2; (2) three assisted ventilation modes: (a) assist-pressure controlled ventilation (APCV1:2) with I:E = 1:2, (b) APCV1:1 with I:E = 1:1; and (c) biphasic positive airway pressure and pressure support ventilation (BiVent + PSV), and (3) spontaneous breathing without PEEP in air. PCV, APCV1:1, and APCV1:2 were set with P (insp) = 10 cmH(2)O and PEEP = 5 cmH(2)O. BiVent + PSV was set with two levels of CPAP [inspiratory pressure (P (High) = 10 cmH(2)O) and positive end-expiratory pressure (P (Low) = 5 cmH(2)O)] and inspiratory/expiratory times: T (High) = 0.3 s and T (Low) = 0.3 s. PSV was set as follows: 2 cmH(2)O above P (High) and 7 cmH(2)O above P (Low). All rats were mechanically ventilated in air and PEEP = 5 cmH(2)O for 1 h. Assisted ventilation modes led to better functional improvement and less lung injury compared to PCV. APCV1:1 and BiVent + PSV presented similar oxygenation levels, which were higher than in APCV1:2. Bivent + PSV led to less alveolar epithelium injury and lower expression of tumour necrosis factor-alpha, interleukin-6, and type III procollagen. In this experimental ALI model, assisted ventilation modes presented greater beneficial effects on respiratory function and a reduction in lung injury compared to PCV. Among assisted ventilation modes, Bi-Vent + PSV demonstrated better functional results with less lung damage and expression of inflammatory mediators.
    European Journal of Intensive Care Medicine 03/2010; 36(8):1417-26. · 5.17 Impact Factor
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    ABSTRACT: A síndrome do desconforto respiratório agudo é caracterizada por uma reação inflamatória difusa do parênquima pulmonar induzida por um insulto direto ao epitélio alveolar (síndrome do desconforto respiratório agudo pulmonar) ou indireto por meio do endotélio vascular (síndrome do desconforto respiratório agudo extrapulmonar). A principal estratégia terapêutica da síndrome do desconforto respiratório agudo é o suporte ventilatório. Entretanto, a ventilação mecânica pode agravar a lesão pulmonar. Nesse contexto, uma estratégia ventilatória protetora com baixo volume corrente foi proposta. Tal estratégia reduziu a taxa de mortalidade dos pacientes com síndrome do desconforto respiratório agudo, porém acarretou acidose hipercápnica. O presente artigo apresenta uma revisão da literatura acerca dos efeitos da acidose hipercápnica na síndrome do desconforto respiratório agudo. Para tal, realizou-se uma revisão sistemática da literatura científica conforme critérios já estabelecidos para análise documental incluindo artigos experimentais e clínicos sobre o tema, usando-se como bases de dados MedLine, LILACS, SciElo, PubMed, Cochrane. A acidose hipercápnica é defendida por alguns autores como moduladora do processo inflamatório da síndrome do desconforto respiratório agudo. Entretanto, estudos clínicos e experimentais acerca dos efeitos da acidose hipercápnica têm demonstrado resultados controversos. Logo, é fundamental a realização de mais pesquisas para elucidar o papel da acidose hipercápnica na síndrome do desconforto respiratório agudo.
    Revista Brasileira de Terapia Intensiva 12/2009; 21(4):404-415.
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    ABSTRACT: To investigate the effects of low and high levels of positive end-expiratory pressure (PEEP), without recruitment maneuvers, during lung protective ventilation in an experimental model of acute lung injury (ALI). Prospective, randomized, and controlled experimental study. University research laboratory. Wistar rats were randomly assigned to control (C) [saline (0.1 mL), intraperitoneally] and ALI [paraquat (15 mg/kg), intraperitoneally] groups. After 24 hours, each group was further randomized into four groups (six rats each) at different PEEP levels = 1.5, 3, 4.5, or 6 cm H2O and ventilated with a constant tidal volume (6 mL/kg) and open thorax. Lung mechanics [static elastance (Est, L) and viscoelastic pressure (DeltaP2, L)] and arterial blood gases were measured before (Pre) and at the end of 1-hour mechanical ventilation (Post). Pulmonary histology (light and electron microscopy) and type III procollagen (PCIII) messenger RNA (mRNA) expression were measured after 1 hour of mechanical ventilation. In ALI group, low and high PEEP levels induced a greater percentage of increase in Est, L (44% and 50%) and DeltaP2, L (56% and 36%) in Post values related to Pre. Low PEEP yielded alveolar collapse whereas high PEEP caused overdistension and atelectasis, with both levels worsening oxygenation and increasing PCIII mRNA expression. In the present nonrecruited ALI model, protective mechanical ventilation with lower and higher PEEP levels than required for better oxygenation increased Est, L and DeltaP2, L, the amount of atelectasis, and PCIII mRNA expression. PEEP selection titrated for a minimum elastance and maximum oxygenation may prevent lung injury while deviation from these settings may be harmful.
    Critical care medicine 04/2009; 37(3):1011-7. · 6.37 Impact Factor
  • Revista Brasileira de Terapia Intensiva 01/2009; 21(4).
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    ABSTRACT: JUSTIFICATIVA E OBJETIVOS: A ventilação mecânica é considerada elemento básico de suporte de vida nas unidades de terapia intensiva e, indubitavelmente, essencial para os pacientes com lesão pulmonar aguda (LPA) e síndrome do desconforto respiratório agudo (SDRA). Estudos experimentais demonstraram que a ventilação mecânica (VM) com altos volumes e/ou altas pressões pode exacerbar ou iniciar uma lesão pulmonar, denominada lesão pulmonar associada à VM (LPAV) ou lesão pulmonar induzida pelo ventilador (LPIV), respectivamente, com aspecto histológico similar ao da LPA/SDRA. CONTEÚDO: Realizou-se uma pesquisa sistemática dos artigos incluídos na MedLine e SciElo dos últimos 20 anos, que abordavam uma visão crítica dos principais mecanismos determinantes da LPIV. Dentre os principais mecanismos da LPAV/LPIV pode-se citar: volutrauma causado por hiperdistensão e expansão desigual das unidades alveolares em função de altas pressões transpulmonares ou volumes; aletectrauma resultante da abertura e fechamento cíclicos das vias aéreas distais e o biotrauma determinado pelo processo inflamatório conseqüente às estratégias ventilatórias lesivas adotadas. CONCLUSÕES: Os mecanismos responsáveis pelo volutrauma, atelectrauma e biotrauma devem ser bem entendidos para que se possa evitar a lesão associada à ventilação mecânica.
    Revista Brasileira de Terapia Intensiva 12/2007; 19(4):469-474.
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    Revista Brasileira de Terapia Intensiva 01/2007; 19(4).