Intraalveolar Expression of Tumor Necrosis Factor- α Gene during Conventional and High-Frequency Ventilation

Takata, Masao; Abe, Jun; Tanaka, Hiroyuki; Kitano, Yoshihiro; Doi, Satomi; Kohsaka, Takao; Miyasaka, Katsuyuki

doi:10.1164/ajrccm.156.1.9607072

Cited by 156 publications

(86 citation statements)

References 30 publications

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“…More recently, experimental studies suggested that mechanical ventilation increases pulmonary levels of inflammatory mediators and induces neutrophil accumulation (14)(15)(16). These studies suggest the hypothesis that ventilator-induced lung injury has an inflammatory component.…”

Section: Introductionmentioning

confidence: 95%

Ventilation with high tidal volume induces inflammatory lung injury

Bueno

Santos

et al. 2002

Braz J Med Biol Res

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Mechanical ventilation with high tidal volumes (V T ) has been shown to induce lung injury. We examined the hypothesis that this procedure induces lung injury with inflammatory features. Anesthetized male Wistar rats were randomized into three groups: group 1 (N = 12): V T = 7 ml/kg, respiratory rate (RR) = 50 breaths/min; group 2 (N = 10): V T = 21 ml/kg, RR = 16 breaths/min; group 3 (N = 11): V T = 42 ml/kg, RR = 8 breaths/min. The animals were ventilated with fraction of inspired oxygen of 1 and positive end-expiratory pressure of 2 cmH 2 O. After 4 h of ventilation, group 3, compared to groups 1 and 2, had lower PaO 2 [280 (range 73-458) vs 517 (range 307-596), and 547 mmHg (range 330-662), respectively, P<0.05], higher wet lung weight [3.62 ± 0.91 vs 1.69 ± 0.48 and 1.44 ± 0.20 g, respectively, P<0.05], and higher wet lung weight/dry lung weight ratio [18.14 (range 11.55-26.31) vs 7.80 (range 4.79-12.18), and 6.34 (range 5.92-7.04), respectively, P<0.05]. Total cell and neutrophil counts were higher in group 3 compared to groups 1 and 2 (P<0.05), as were baseline TNF-α concentrations [134 (range <10-386) vs 16 (range <10-24), and 17 pg/ml (range <10-23), respectively, P<0.05]. Serum TNF-α concentrations reached a higher level in group 3, but without statistical significance. These results suggest that mechanical ventilation with high V T induces lung injury with inflammatory characteristics. This ventilatory strategy can affect the release of TNF-α in the lungs and can reach the systemic circulation, a finding that may have relevance for the development of a systemic inflammatory response.

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Section: Introductionmentioning

confidence: 95%

Ventilation with high tidal volume induces inflammatory lung injury

Bueno

Santos

et al. 2002

Braz J Med Biol Res

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“…Os benefícios da HFO na SARA poderiam ser atribuídos a dois fatores: a manutenção de uma pressão constante nas vias aéreas e o uso de diminutos volumes correntes 11,17,20,31 . Esses dois fatores têm como principais vantagens evitar o colapso pulmonar progressivo (mantêm a estabilidade alveolar), evitar grandes oscilações no volume alveolar (previnem a distensão e o colapso alveolar), poupar surfactante e diminuir o processo inflamatório local 2,5,6,11,13,18,20,21,31 .…”

Section: Antes De Discutirmos Esses Resultados Julgamos Pertinente Qunclassified

“…Apesar dos estudos clínicos em humanos serem ainda controversos, a HFO vem sendo reconhecida com uma alternativa eficaz para ser empregada em insuficiência respiratória da criança e do recém nascido. Estudos clínicos têm sugerido que a HFO estaria associada como uma menor incidência de lesão pulmonar induzida que a ventilação convencional 5,13,16,18,21 .…”

Section: Introductionunclassified

High frequency oscillation ventilation compared to conventional mechanical ventilation plus exogenous surfactant replacement in rabbits

Piva¹,

Chatrkaw²,

Choong³

et al. 2000

J Pediatr (Rio J)

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ResumoObjetivos: a) avaliar o efeito na oxigenação e ventilação de coelhos artificialmente depletados de surfactante quando submetidos à ventilação mecânica convencional associada à reposição parcial de surfactante exógeno; b) comparar a evolução deste grupo com outro grupo submetido à ventilação de alta freqüência por oscilação (HFO) sem reposição associada de surfactante.Métodos: Vinte coelhos brancos da raça New Zealand, peso de + 3 kg, foram anestesiados e artificialmente induzidos à depleção de surfactante endógeno através de sucessivas lavagens pulmonares com alíquotas (25 ml/kg) de solução fisiológica, até atingir uma PaO 2 menor que 100 mmHg, quando ventilados via traqueostomia no modo de pressão controlada objetivando um volume corrente de 10ml/kg, com PEEP de 5cm H 2 O, FiO 2 de 100%, freqüência respiratória de 30 mpm, e tempo inspiratório de 0,65 s. Posteriormente, os coelhos foram divididos em (a) grupo CMV+S, submetido à ventilação convencional associada com reposição parcial de surfactante exógeno; (b) grupo HFO submetido à ventilação de alta freqüência por oscilação. Gasometrias arteriais foram coletadas antes da lavagem pulmonar, após a lavagem pulmonar, 15, 60 e 120 minutos após iniciado o tratamento. Os grupos foram comparados utilizando-se o teste t de Student.Resultados: Em ambos grupos a PaO 2 (pós lavagem pulmonar) era inferior a 50mmHg (p=0,154), subindo aos15 minutos de tratamento para 254 mmHg (CMV+S) e 288 mmHg (HFO, p=0,626). Aos 60 e 120 minutos, a PaO 2 foi maior (p=0,001) no grupo HFO (431 e 431 mmHg) quando comparado com o grupo CMV+S, que apresentou queda progressiva (148 e 126 mmHg). Aos 60 minutos a PaCO 2 era significativamente menor no grupo do CMV+S (29 versus 41 mmHg).Conclusões: Em modelo animal com SARA a estratégia de ventilação protetora como a HFO, isoladamente, promove uma rápida e persistente melhora na oxigenação, inclusive, com níveis superiores aos obtidos pelos animais submetidos à ventilação mecâ-nica convencional associada à reposição de surfactante. AbstractObjectives: (a) to evaluate the effect on oxygenation and ventilation of rabbits with induced surfactant depletion when they are submitted to a conventional mechanical ventilation, plus a small dose of exogenous surfactant; (b) to compare this group with another group submitted to a High Frequency Oscillation (HFO) without exogenous surfactant administration.Methods: Twenty New Zealand White rabbits weighing (+ 3 kg) were anaesthetized and artificially induced to a endogenous surfactant depletion by successively lung lavage with normal saline (aliquots of 25 ml/kg) until to reach a persistent PaO 2 less than 100 mmHg when submitted to a mechanical ventilation in a pressure control mode with a target tidal volume of 10ml/kg, PEEP of 5cm H 2 O, FiO 2 1.0, respiratory rate 30/min, and inspiratory time of 0.65 s. Then the rabbits were divided in (a) CMV+S group, submitted to a conventional mechanical ventilation plus exogenous surfactant replacement; (b) HFO group, submitted to a High Frequency Oscillation Vent...

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“…Many RCTs have studied the pattern of inflammatory cytokines in the broncho-alveolar lavage (BAL) and/or blood in patients with non-ARDS, when patients were ventilated at conventional V T compared to protective V T of 6 ml/kg PBW, studies showed that these markers had a sustained increase in the former group 7 . Experimentally, inflammatory markers increase as early as 1 hour after initiation of ventilation 8,9 . It has also been shown in animal models that volume and not the high airway pressure is responsible for increasing the alveolar permeability 10 .…”

Section: Commentarymentioning

confidence: 99%