Intratracheal anti-tumor necrosis factor-α antibody attenuates ventilator-induced lung injury in rabbits

Imai, Yumiko; Kawano, Tsuyoshi; Iwamoto, Satoshi; Nakagawa, Satoshi; Takata, Masao; Miyasaka, Katsuyuki

doi:10.1152/jappl.1999.87.2.510

Cited by 134 publications

(72 citation statements)

References 23 publications

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“…Following acid aspirationinduced lung injury in rats, higher tidal volumes are associated with greater increases in plasma and BAL TNF-α and MIP-2 12 and plasma IL-1β 56 than acid injury alone or noninjurious ventilation. Others 13,14,57,58 have reported similar results in surfactant-depleted rats, rabbits, and pigs ventilated with high or low tidal volume or high-frequency oscillatory ventilation. Antibody blockade of TNF-α decreased histopathologic lung injury in surfactant-depleted rats, 13 while blockade of IL-1 with IL-1Ra attenuated lung injury after 8 h of ventilation in surfactant-depleted rabbits.…”

Section: Cytokines and Chemokines In Experimental Studiesmentioning

confidence: 63%

“…Others 13,14,57,58 have reported similar results in surfactant-depleted rats, rabbits, and pigs ventilated with high or low tidal volume or high-frequency oscillatory ventilation. Antibody blockade of TNF-α decreased histopathologic lung injury in surfactant-depleted rats, 13 while blockade of IL-1 with IL-1Ra attenuated lung injury after 8 h of ventilation in surfactant-depleted rabbits. 24 These data suggest a pathogenetic role for TNF-α and IL-1 in VALI.…”

Section: Cytokines and Chemokines In Experimental Studiesmentioning

confidence: 63%

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Pathogenetic Significance of Biological Markers of Ventilator-Associated Lung Injury in Experimental and Clinical Studies

Frank

Parsons

Matthay

2006

Chest

114

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For patients with acute lung injury, positive pressure mechanical ventilation is life saving. However, considerable experimental and clinical data have demonstrated that how clinicians set the tidal volume, positive end-expiratory pressure, and plateau airway pressure influences lung injury severity and patient outcomes including mortality. In order to better identify ventilator-associated lung injury (VALI), clinical investigators have sought to measure blood-borne and airspace biological markers of VALI. At the same time, several laboratory-based studies have focused on biological markers of inflammation and organ injury in experimental models in order to clarify the mechanisms of ventilator-induced lung injury (VILI) and VALI. This review summarizes data on biological markers of VALI and VILI from both clinical and experimental studies with an emphasis on markers identified in patients and in the experimental setting. This analysis suggests that measurement of some of these biological markers may be of value in diagnosing VALI and in understanding its pathogenesis. Keywords ARDS; critical care; ventilation; ventilator-induced lung injuryAlthough clinicians and researchers have been interested in ventilator-induced lung injury (VILI) for at least 30 years, the reduction in mortality associated with low tidal volume ventilation in patients with acute lung injury (ALI) and ARDS 1 has directed increasing scientific interest toward the mechanisms of VILI. One of the greatest difficulties in clinical studies has been distinguishing the underlying lung injury responsible for the patient's respiratory failure from the lung injury resulting from the particular settings of the mechanical ventilator. Consequently, investigators have searched for biological markers that will reflect ventilator-attributable lung injury. The term VILI generally refers to experimental models in which lung injury in induced directly by an injurious ventilation strategy. Ventilator-associated lung injury (VALI) refers to the additional injury imposed on a previously injured lung by mechanical ventilation in either the clinical setting or in experimental studies. For the purposes of this review, the term ventilator-attributable injury encompasses all of these types of injury. Researchers have used a variety of experimental models to determine the effects of mechanical ventilation or mechanical strain on the expression of biological markers of inflammation or Biologic Markers of Inflammation in Clinical StudiesThe role of the innate immune response and inflammation in the pathogenesis of VILI has been widely studied in recent years. Although some have suggested that inflammation may not be integral to the initiation of VILI, clearly a preponderance of data in this field support a major pathogenetic role for inflammation and lung neutrophil recruitment. The majority of biological markers identified in plasma, serum, pulmonary edema fluid, and BAL fluid in experimental studies are cytokines and chemokines. Although none of these mediator...

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Section: Cytokines and Chemokines In Experimental Studiesmentioning

confidence: 63%

Section: Cytokines and Chemokines In Experimental Studiesmentioning

confidence: 63%

Pathogenetic Significance of Biological Markers of Ventilator-Associated Lung Injury in Experimental and Clinical Studies

Frank

Parsons

Matthay

2006

Chest

114

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“…Recentemente, tem sido demonstrado na literatura que mediadores inflamatórios, como o FNT-alfa e as interleucinas, aumentam durante a ventilação mecânica, principalmente quando se empregam volumes correntes elevados 13,14,[21][22][23][24][25] . Naik et al observaram que o início da ventilação mecânica em ovelhas prematuras desencadeou o aumento dos níveis de mediadores inflamatórios, sugerindo que bastam alguns ciclos de ventilação mecâ-nica no prematuro para causar a lesão pulmonar 15 .…”

Section: Reação Inflamatóriaunclassified

Strategies to minimize lung injury in extremely low birth weight infants

Suguihara¹,

Lessa²

2005

J Pediatr (Rio J)

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Como citar este artigo: Suguihara C, Lessa AC. Como minimizar a lesão pulmonar no prematuro extremo: propostas. J Pediatr (Rio J). 2005;81(1 Supl):S69-S78. AbstractObjective: To review the main causes of new bronchopulmonary dysplasia and the strategies utilized to decrease its incidence in extremely low birth weight infants. Sources of data:For this review a MEDLINE search from 1966 to October 2004, the Cochrane Database, abstracts from the Society for Pediatric Research and recent meetings on the topic were used. Summary of the findings:The survival of extremely low birth weight infants has increased significantly due to improvement in both scientific knowledge and technology. This improvement in survival has therefore resulted in an increased incidence of bronchopulmonary dysplasia. The characteristics of bronchopulmonary dysplasia in extremely low birth weight infants, the so called new bronchopulmonary dysplasia are quite different from the classic bronchopulmonary dysplasia described by Northway. This new bronchopulmonary dysplasia has a multifactorial etiology, which includes volutrauma, atelectrauma, oxygen toxicity and lung inflammation. Therapy such as prenatal corticosteroids, exogenous surfactant, nasal continuous positive airway pressure, new mechanical ventilation modalities and gentle ventilation have been used in attempts to decrease lung injury severity. Conclusions:In order to prevent lung injury in extremely low birth weight infants, it is necessary to minimize several factors that induce bronchopulmonary dysplasia and to utilize less aggressive therapeutic strategies. In addition to the current therapy used to decrease lung injury, knowledge of these causative factors may create new therapies that may be fundamental in improving the clinical outcomes of premature infants.J Pediatr (Rio J). 2005;81(1 Supl):S69-S78: Extremely low birth weight infant, bronchopulmonary dysplasia, mechanical ventilation. ResumoObjetivo: Apresentar uma revisão das principais causas da nova displasia broncopulmonar e as estratégias utilizadas para diminuir sua incidência nos prematuros extremos. Fontes dos dados:Para essa revisão, pesquisas foram feitas na MEDLINE (1996 a outubro de 2004), no Cochrane Database, em resumos da Society for Pediatric Research e recentes conferências sobre o tema. Síntese dos dados:A tecnologia e os novos conhecimentos científicos têm aumentado significantemente a sobrevida de prematuros extremos. Esse aumento da sobrevida resultou em aumento da incidência de displasia broncopulmonar. Atualmente, a displasia broncopulmonar é mais freqüentemente observada em recém-nascidos < 1.200 g. As características da displasia broncopulmonar nesses prematuros extremos, atualmente chamada de nova displasia broncopulmonar, são bastante diferentes da clássica descrita por Northway. A nova displasia broncopulmonar tem etiologia multifatorial, como volutrauma, atelectrauma, toxicidade ao oxigênio e reação inflamatória. Terapias como corticosteróide pré-natal, surfactante exógeno, pressão aérea positiva co...

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“…Studies on lung lavage have shown increased levels of tumor necrosis factor-alpha (TNF-α), interleukins (IL)-1ß, -6 and -10, interferon-γ and thromboxane ß2, suggesting an ongoing pulmonary inflammatory response (4)(5)(6) that is often associated with the migration of neutrophils to the lung (7).…”

Section: Introductionmentioning

confidence: 99%

Pentoxifylline decreases tumor necrosis factor and interleukin-1 during high tidal volume

Oliveira-Júnior

Pinheiro

Silva

et al. 2003

Braz J Med Biol Res

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Tumor necrosis factor-alpha (TNF-α) is one of the most important proinflammatory cytokines which plays a central role in host defense and in the acute inflammatory response related to tissue injury. The major source of TNF-α are immune cells such as neutrophils and macrophages. We tested the hypothesis that pentoxifylline, a methylxanthine derivative, down-regulates proinflammatory cytokine expression during acute lung injury in rats. Male Wistar rats weighing 250 to 450 g were anesthetized ip with 50 mg/kg sodium thiopental and randomly divided into three groups: group 1 (N = 7): tidal volume (V T ) = 7 ml/kg, respiratory rate (RR) = 50 breaths/min and normal saline infusion; group 2 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and normal saline infusion; group 3 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and pentoxifylline infusion. The animals were ventilated with an inspired oxygen fraction of 1.0, a positive end-expiratory pressure of 3 cmH 2 O, and normal saline or pentoxifylline injected into the left femoral vein. The mRNA of TNF-α rapidly increased in the lung tissue within 180 min of ventilation with a higher V T with normal saline infusion. The concentrations of inflammatory mediators were decreased in plasma and bronchoalveolar lavage (BAL) in the presence of higher V T with pentoxifylline infusion (TNF-α: plasma, 102.2 ± 90.9 and BAL, 118.2 ± 82.1; IL-1ß: plasma, 45.2 ± 42.7 and BAL, 50.2 ± 34.9, P < 0.05). We conclude that TNF-α produced by neutrophil influx may function as an alert signal in host defense to induce production of other inflammatory mediators.

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Intratracheal anti-tumor necrosis factor-α antibody attenuates ventilator-induced lung injury in rabbits

Cited by 134 publications

References 23 publications

Pathogenetic Significance of Biological Markers of Ventilator-Associated Lung Injury in Experimental and Clinical Studies

Pathogenetic Significance of Biological Markers of Ventilator-Associated Lung Injury in Experimental and Clinical Studies

Strategies to minimize lung injury in extremely low birth weight infants

Pentoxifylline decreases tumor necrosis factor and interleukin-1 during high tidal volume

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