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                     <i>Desflurane Increases Pulmonary Alveolar-Capillary Membrane Permeability after Aortic Occlusion-Reperfusion in Rabbits</i> </b>

Nielsen, Vance G.; Baird, Manuel S.; McAdams, Michelle; Freeman, Bruce Α.

doi:10.1097/00000542-199806000-00017

Cited by 28 publications

(7 citation statements)

References 35 publications

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“…Nonpulmonary I/R: the nonpulmonary I/R model has been used mainly in rats and mice, although there are some studies in rabbits (8,150) and sheep (116,195). Models differ in terms of the anatomic area subjected to ischemia, e.g., gut, liver, kidneys, lower torso, the duration of the ischemic period, and the duration of reperfusion.…”

Section: Models Targeting the Epithelium And Endotheliummentioning

confidence: 99%

Animal models of acute lung injury

Matute-Bello

Frevert

Martin

2008

American Journal of Physiology-Lung Cellular and Molecular Phys

1,440

1,397

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Acute lung injury in humans is characterized histopathologically by neutrophilic alveolitis, injury of the alveolar epithelium and endothelium, hyaline membrane formation, and microvascular thrombi. Different animal models of experimental lung injury have been used to investigate mechanisms of lung injury. Most are based on reproducing in animals known risk factors for ARDS, such as sepsis, lipid embolism secondary to bone fracture, acid aspiration, ischemia-reperfusion of pulmonary or distal vascular beds, and other clinical risks. However, none of these models fully reproduces the features of human lung injury. The goal of this review is to summarize the strengths and weaknesses of existing models of lung injury. We review the specific features of human ARDS that should be modeled in experimental lung injury and then discuss specific characteristics of animal species that may affect the pulmonary host response to noxious stimuli. We emphasize those models of lung injury that are based on reproducing risk factors for human ARDS in animals and discuss the advantages and disadvantages of each model and the extent to which each model reproduces human ARDS. The present review will help guide investigators in the design and interpretation of animal studies of acute lung injury.

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Section: Models Targeting the Epithelium And Endotheliummentioning

confidence: 99%

Animal models of acute lung injury

Matute-Bello

Frevert

Martin

2008

American Journal of Physiology-Lung Cellular and Molecular Phys

1,440

1,397

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“…At the completion of this experiment, the BALF concentration of LDH in the DES-IR group was higher than in the other groups. This indicated not only the decreased functions of the vascular endothelium, but also damage to lung tissue (Nielsen et al 1998). …”

Section: Discussionmentioning

confidence: 99%

“…Desflurane has a chemical formula similar to that of isoflurane (Eger 1987), but it has more potent stimulatory effects on the sympathetic nerve than isoflurane (Weiskopf et al 1994). In addition, the blocked thoracic aorta causes oxidative stress in the entire organism through ischemia and subsequently pulmonary vascular permeability, which is exacerbated by desflurane (Nielsen et al 1998). In addition, in pigs under mechanical ventilation, desflurane (1 minimum alveolar concentration [MAC]) inhalation caused oxidative stress in the lungs and induced the apoptosis of lung cells (Allaouchiche et al 2001; Kalimeris et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Desflurane inhalation before ischemia increases ischemia–reperfusion-induced vascular leakage in isolated rabbit lungs

et al. 2016

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BackgroundIsoflurane and sevoflurane protect lungs with ischemia–reperfusion (IR) injury. We examined the influence of desflurane on IR lung injury using isolated rabbit lungs perfused with a physiological salt solution.MethodsThe isolated lungs were divided into three groups: IR, desflurane-treated ischemia–reperfusion (DES-IR), and ventilation/perfusion-continued control (Cont) groups (n = 6 per group). In the DES-IR group, inhalation of desflurane at 1 minimum alveolar concentration (MAC) was conducted in a stable 30-min phase. In the IR and DES-IR groups, ventilation/perfusion was stopped for 75 min after the stable phase. Subsequently, they were resumed. Each lung was placed on a balance, and weighed. Weight changes were measured serially throughout this experiment. The coefficient of filtration (Kfc) was determined immediately before ischemia and 60 min after reperfusion. Furthermore, bronchoalveolar lavage fluid (BALF) was collected from the right bronchus at the completion of the experiment. After the completion of the experiment, the left lung was dried, and the lung wet-to-dry weight ratio (W/D) was calculated.ResultsThe Kfc values at 60 min after perfusion were 0.40 ± 0.13 ml/min/mmHg/100 g in the DES-IR group, 0.26 ± 0.07 ml/min/mmHg/100 g in the IR group, and 0.22 ± 0.08 (mean ± SD) ml/mmHg/100 g in the Cont group. In the DES-IR group, the Kfc at 60 min after the start of reperfusion was significantly higher than in the other groups. In the DES-IR group, W/D was significantly higher than in the Cont group. In the DES-IR group, the BALF concentrations of nitric oxide metabolites were significantly higher than in the other groups. In the DES-IR group, the total amount of vascular endothelial growth factor in BALF was significantly higher than in the Cont group.ConclusionsThe pre-inhalation of desflurane at 1 MAC exacerbates pulmonary IR injury in isolated/perfused rabbit lungs.

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“…Many clinical and experimental studies also demonstrated that hepatoenteric ischemiareperfusion caused significant pulmonary injuries (2,5,(33)(34)(35)(36). Activation of neutrophils and their sequestration and adherence to the pulmonary endothelium are important steps in the development of a pulmonary microvascular permeability increase.…”

Section: Discussionmentioning

confidence: 99%

Sivelestat, a Neutrophil Elastase Inhibitor, Attenuates Neutrophil Priming After Hepatoenteric Ischemia in Rabbits

Kotake¹,

Yamamoto²,

Matsumoto

et al. 2005

Shock

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Neutrophils play an important role in ischemia-reperfusion injury. The neutrophil elastase not only causes tissue damage, but also mediates neutrophil priming. In the present study, we use a rabbit model of hepatoenteric ischemia-reperfusion to test the hypothesis that neutrophil elastase inhibition ameliorates an ischemia-reperfusion injury by attenuating neutrophil priming and suppressing enzymatic activity. Twenty-four Japanese white rabbits underwent 30 min of supraceliac aortic cross-clamping and 180 min of reperfusion under isoflurane anesthesia. The rabbits randomly received the neutrophil elastase inhibitor, sivelestat (n = 10), or saline (n = 14). Neutrophil priming was then assayed with luminol-dependent neutrophil chemiluminescence. Hepatic, intestinal, renal, and pulmonary damages were assessed with serum transaminase, lactate dehydrogenase concentrations, urinary N-acetyl glucosaminidase activity, and protein concentration in post mortem bronchoalveolar lavage fluid. We discovered that neutrophil elastase inhibition suppressed plasma neutrophil elastase, and that lipid peroxide concentrations increased after reperfusion. It improved ischemia-reperfusion injuries in the liver, intestine, kidney, and lung. Furthermore, inhibition of neutrophil elastase with sivelestat significantly attenuated post-reperfusion neutrophil priming. The results of this study demonstrate that neutrophil elastase inhibition could effectively attenuate an ischemia-reperfusion injury caused by supraceliac aortic cross-clamping, most likely from the attenuation of neutrophil priming.

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Desflurane Increases Pulmonary Alveolar-Capillary Membrane Permeability after Aortic Occlusion-Reperfusion in Rabbits

Abstract: Desflurane anesthesia increased xanthine oxidase-dependent alveolar-capillary membrane compromise after aortic occlusion-reperfusion in concert with depletion of a key tissue antioxidant.

Cited by 28 publications

References 35 publications

Animal models of acute lung injury

Animal models of acute lung injury

Desflurane inhalation before ischemia increases ischemia–reperfusion-induced vascular leakage in isolated rabbit lungs

Sivelestat, a Neutrophil Elastase Inhibitor, Attenuates Neutrophil Priming After Hepatoenteric Ischemia in Rabbits

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