Effect of surfactant on respiratory failure associated with thoracic aneurysm surgery

Satoh, Daizoh; Matsukawa, Shu; Saishu, Toshio; Hashimoto, Yoshiaki

doi:10.1097/00003246-199810000-00017

Cited by 9 publications

(4 citation statements)

References 10 publications

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“…These results suggest that the protective effects of NADPH oxidase inhibition were not mediated through prevention of CPB-induced surfactant dysfunction (19,37,51) or attenuation of the increased pulmonary vascular protein permeability observed in control animals. The interpretation of the EVLW data is more complicated, because the values shown in Fig.…”

Section: Discussionmentioning

confidence: 80%

Effect of NADPH oxidase inhibition on cardiopulmonary bypass-induced lung injury

Dodd‐o

Welsh

Salazar

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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. Effect of NADPH oxidase inhibition on cardiopulmonary bypass-induced lung injury. Am J Physiol Heart Circ Physiol 287: H927-H936, 2004; 10.1152/ajpheart.01138.2003.-Cardiopulmonary bypass (CPB) causes acute lung injury. Reactive oxygen species (ROS) from NADPH oxidase may contribute to this injury. To determine the role of NADPH oxidase, we pretreated pigs with structurally dissimilar NADPH oxidase inhibitors. Low-dose apocynin (4-hydroxy-3-methoxy-acetophenone; 200 mg/kg, n ϭ 6), highdose apocynin (400 mg/kg, n ϭ 6), or diphenyleneiodonium (DPI; 8 mg/kg) was compared with diluent (n ϭ 8). An additional group was treated with indomethacin (10 mg/kg, n ϭ 3). CPB was performed for 2 h with deflated lungs, complete pulmonary artery occlusion, and bronchial artery ligation to maximize lung injury. Parameters of pulmonary function were evaluated for 25 min following CPB. Blood chemiluminescence indicated neutrophil ROS production. Electron paramagnetic resonance determined the effect of apocynin and DPI on in vitro pulmonary endothelial ROS production following hypoxiareoxygenation. Both apocynin and DPI attenuated blood chemiluminescence and post-CPB hypoxemia. At 25 min post-CPB with FI O 2 ϭ 1, arterial PO2 (PaO 2 ) averaged 52 Ϯ 5, 162 Ϯ 54, 335 Ϯ 88, and 329 Ϯ 119 mmHg in control, low-dose apocynin, high-dose apocynin, and DPI-treated groups, respectively (P Ͻ 0.01). Indomethacin had no effect. PaO 2 correlated with blood chemiluminescence measured after drug administration before CPB (R ϭ Ϫ0.60, P Ͻ 0.005). Neither apocynin nor DPI prevented the increased tracheal pressure, plasma cytokine concentrations (tumor necrosis factor-␣ and IL-6), extravascular lung water, and pulmonary vascular protein permeability observed in control pigs. NADPH oxidase inhibition, but not xanthine oxidase inhibition, significantly blocked endothelial ROS generation following hypoxia-reoxygenation (P Ͻ 0.05). NADPH oxidase-derived ROS contribute to the severe hypoxemia but not to the increased cytokine generation and pulmonary vascular protein permeability, which occur following CPB. diphenyleneiodonium; apocynin; reflection coefficient; pig; endothelium; hypoxia-reoxygenation; tumor necrosis factor; interleukin-6 CARDIOPULMONARY BYPASS (CPB) causes significant lung injury characterized by abnormal gas exchange and pulmonary edema (61). Pulmonary dysfunction results in a mortality rate of nearly 0.7% following cardiac surgery (12, 28), accounting for over half of the 1.3% overall mortality associated with this procedure (11). Proposed mechanisms behind CPB-induced lung injury include the adverse effects of pulmonary vascular ischemia and reperfusion (18), and, if the lung is deflated during CPB, tissue hypoxia and reoxygenation (18, 33). The generation of reactive oxygen species (ROS) is common to all of these injurious mechanisms and is thought to play an important role in the ensuing injury. Sources of ROS include activated inflammatory cells, such as neutrophils (44) and macrophages, as well as vascular endothelial cells subject...

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Section: Discussionmentioning

confidence: 80%

Effect of NADPH oxidase inhibition on cardiopulmonary bypass-induced lung injury

Dodd‐o

Welsh

Salazar

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Anticoagulants exert anti-inflammatory as well as anticoagulant properties which may be utilized to protect against lung injury and ARDS. It is therefore reasoned that an early intervention with surfactant replacement with adjunctive fibrinolytic or thrombolytic anticoagulant agents may alter the clinical course and phenotypical expression of the ALI/ARDS disease pattern [201,207].…”

Section: Microthrombosis and A Role For Anticoagulants And Thrombolysis With Or Without Surfactant As Treatment Agents In Covid-19 And VImentioning

confidence: 99%

An overview of acute lung injury in general and in particular viral infections with specific reference to nebulized surfactant and anticoagulation

Smith¹,

Coetzee²,

Zyl³

2020

J Respir Dis Med

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The coronavirus 2 (SARS-CoV-2) has resulted in an international pandemic. The SARS-CoV-2 affects cardiovascular, digestive and urogenital systems. In an attempt to develop a multimodal and targeted approach to the pathophysiology associated with viral lung injury, we reviewed lung histopathology, inflammation, surfactant biology and pathophysiology related to viral associated acute lung injury (ALI / ARDS). Histopathology of viral pneumonia/ARDS cases of the past 100 years has revealed that lung parenchymal and vascular pathologic changes described in the 1918 influenza pandemic, are no different from the histopathology observed in other viral pandemics. Given the inflammatory storm which can occur in COVID-19 infection, the patient is a candidate to develop the classic multi-organ dysfunction and / or failure (MOD/F) which may well include ALI and ARDS. Because there is a well described temporal change in the pathophysiology associated with ALI /ARDS, a "one size fit al" remedy will not suffice, hence our attempt at a targeted functional approach. For instance, variable results in adults treated with surfactant have relegated the use of surfactant in adult ARDS to an uncertainty. We speculate that early and repeated surfactant installation in adults is required in adults. Surfactant may also have beneficial effects on the inflammatory process in the ARDS lung. The increased clotting tendency associated with the inflammation (and ARDS), particularly the effect on the lung vasculature (acute pulmonary hypertension and increased dead space), causes mechanical pressure overload (and failure) of the right ventricle and mechanical respiratory failure. Active management of these should include inhibition of the accelerated coagulation and thrombolysis (via nebulization) and early inotropic support.

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“…Few data are available on the efficacy of surfactant therapy in patients developing ARDS after cardiac surgery (Satoh et al, 1998;Hermon et al, 2002). In 19 children with ARDS (6 of them after open heart surgery) who received surfactant administration at a dose of 50-100 mg/kg, Hermon et al (2002) noted that there was no improvement in gas exchange, with the mortality rate of 50%.…”

Section: Introductionmentioning

confidence: 99%

“…In 19 children with ARDS (6 of them after open heart surgery) who received surfactant administration at a dose of 50-100 mg/kg, Hermon et al (2002) noted that there was no improvement in gas exchange, with the mortality rate of 50%. The results of another study (Satoh et al, 1998) investigating the effect of the administration of 30 mg/kg Surfactant TA in 11 patients (6 patients randomized to the therapeutic and 5 patients to the control group) with ARDS after resection of aneurism of thoracic aorta also showed significant improvement in oxygenation, but no data on the mortality rate were presented.…”

Section: Introductionmentioning

confidence: 99%

Surfactant Therapy for Patients with ARDS After Cardiac Surgery

Баутин

Хубулава

Kozlov

et al. 2006

Journal of Liposome Research

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Effect of surfactant on respiratory failure associated with thoracic aneurysm surgery

Abstract: Surfactant administration immediately after surgery restored gas exchange in postoperative respiratory failure associated with thoracic aneurysm surgery.

Cited by 9 publications

References 10 publications

Effect of NADPH oxidase inhibition on cardiopulmonary bypass-induced lung injury

Effect of NADPH oxidase inhibition on cardiopulmonary bypass-induced lung injury

An overview of acute lung injury in general and in particular viral infections with specific reference to nebulized surfactant and anticoagulation

Surfactant Therapy for Patients with ARDS After Cardiac Surgery

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