Propofol attenuates oxidant-induced acute lung injury in an isolated perfused rabbit-lung model

Yumoto, Masato; Nishida, Osamu; Nakamura, Fujio; Hikita, Katsuya

doi:10.1007/s00540-005-0338-9

Cited by 12 publications

(9 citation statements)

References 21 publications

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“…Specifically, we have previously shown that systemic lipid oxidation during IIR mediates altered lipid metabolism and increased alveolocapillary permeability in the lung [4]. Based on these results, we investigated propofol as a preventive agent because of its potent ability to inhibit lipid oxidation and suppress lipid metabolism [12,21] . Indeed, propofol was efficient in restoring TBARS levels to the baseline values, thus providing important antioxidant protection.…”

Section: Discussionmentioning

confidence: 97%

“…Propofol (2, 6-diisopropyl phenol) is a commonly used intravenous anesthetic that is chemically similar to a-tocopherol and possesses potent antioxidant properties [9]. In addition to its ability to specifically counteract ischemia/reperfusion-induced lipid peroxidation [10,11], propofol also attenuates lung injury from both direct and remotely produced oxidants [12,13]. These benefits offered by propofol, along with the widespread use of the drug in the anesthetic practice, prompted us to test its efficacy in the prevention of lung injury following IIR.…”

Section: Introductionmentioning

confidence: 99%

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Propofol Prevents Lung Injury Following Intestinal Ischemia-Reperfusion

Vasileiou

Kalimeris

Nomikos

et al. 2012

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Propofol Prevents Lung Injury Following Intestinal Ischemia-Reperfusion

Vasileiou

Kalimeris

Nomikos

et al. 2012

Journal of Surgical Research

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“…Propofol (2,6‐diisopropylphenol), an intravenous sedative–hypnotic agent popular for sedation, is chemically similar to phenol‐based free‐radical scavengers such as the endogenous antioxidant vitamin E, while its lipophilic nature allows its rapid access to cellular and subcellular membranes compartments. Propofol has been found to be effective in protecting against pathological states characterized by an increase in basal rate of ROS production in brain ( Lee et al , 2005 ), lung ( Yumoto et al , 2005 ), liver ( Tsao et al , 2003 ), testicle ( Unsal et al , 2004 ) and hearts ( Xia et al , 1996 ), but the mechanism by which it exerts the cardioprotective effect is not well established. In the current study, we propose that propofol treatment will decrease cardiac ischaemia and reperfusion injury by preservation of mitochondrial function via prevention of cardiolipin peroxidation at the mitochondrial level.…”

Section: Introductionmentioning

confidence: 99%

Dose‐dependent protective effect of propofol against mitochondrial dysfunction in ischaemic/reperfused rat heart: role of cardiolipin

Shao

Zhou

et al. 2008

British J Pharmacology

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Background and purpose: Ischaemia damages to the cardiac mitochondria by increasing generation of reactive oxygen species (ROS) and peroxidation of cardiolipin. The inhibited mitochondrial function leads to the cardiac injury during reperfusion. Propofol (2, 6-diisopropylphenol), an intravenous anaesthetic, has been shown to decrease cardiac ischaemia and reperfusion injury. In the present study, we propose that propofol protects mitochondrial function and decreases cardiac injury by prevention of cardiolipin peroxidation during ischaemia and reperfusion. Experimental approach: After isolation of mitochondria from isolated rat heart perfused on a Langendorff model, various mitochondrial bioenergetic parameters were evaluated such as rates of mitochondrial oxygen consumption, H 2 O 2 production, complex I and III activity as well as the degree of lipid peroxidation and cardiolipin content. The action of propofol was also explored in isolated mitochondria. And the effect of cardiolipin was evaluated by fusing cardiolipin liposome with mitochondria. Key results: Propofol treatment had strong dose-dependent protection attenuating these parameters alterations in reperfused rat heart and isolated mitochondria. Additionally, cardiolipin treatment had the same protective effect, compared with propofol treatment at high concentration. Conclusions and implications:The protective effect of propofol appears to be due, at least in part, as a chemical uncoupler, to the interruption of the vicious circle of ROS-cardiolipin-complexes of the respiratory chain-ROS through preserving the content and integrity of cardiolipin molecules by ROS attack. These findings may provide an explanation for some of the factors responsible for cardioprotection and one approach exploring an available antioxidant.

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“…An index of Kf was determined from the changes in lung weight(LW) induced by elevated PVP as previously described[13]. During ventilation and perfusion, the PVP was rapidly elevated by 10 cm H 2 O for 7 minutes.…”

Section: Methodsmentioning

confidence: 99%

“…The slow, and steady phase of LW gain as a function of time (ΔW/ΔT) was plotted on a semi-logarithmic scale and then extrapolated to time zero to obtain the initial rate of trans-capillary filtration. From this plot, Kf was defined as the y-intercept (gm/min) divided by PVP (10 cm H 2 O) and LW (gm), and expressed in whole units of grams per minute per centimeter of H 2 O multiplied by 100 g[13]. …”

Section: Methodsmentioning

confidence: 99%

Carbonic anhydrase inhibitor attenuates ischemia-reperfusion induced acute lung injury

et al. 2017

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Ischemia-reperfusion (IR)-induced acute lung injury (ALI) is implicated in several clinical conditions including lung transplantation, cardiopulmonary bypass surgery, re-expansion of collapsed lung from pneumothorax or pleural effusion and etc. IR-induced ALI remains a challenge in the current treatment. Carbonic anhydrase has important physiological function and influences on transport of CO2. Some investigators suggest that CO2 influences lung injury. Therefore, carbonic anhydrase should have the role in ALI. This study was undertaken to define the effect of a carbonic anhydrase inhibitor, acetazolamide (AZA), in IR-induced ALI, that was conducted in a rat model of isolated-perfused lung with 30 minutes of ischemia and 90 minutes of reperfusion. The animals were divided into six groups (n = 6 per group): sham, sham + AZA 200 mg/kg body weight (BW), IR, IR + AZA 100 mg/kg BW, IR + AZA 200 mg/kg BW and IR+ AZA 400 mg/kg BW. IR caused significant pulmonary micro-vascular hyper-permeability, pulmonary edema, pulmonary hypertension, neutrophilic sequestration, and an increase in the expression of pro-inflammatory cytokines. Increases in carbonic anhydrase expression and perfusate pCO2 levels were noted, while decreased Na-K-ATPase expression was noted after IR. Administration of 200mg/kg BW and 400mg/kg BW AZA significantly suppressed the expression of pro-inflammatory cytokines (TNF-α, IL-1, IL-6 and IL-17) and attenuated IR-induced lung injury, represented by decreases in pulmonary hyper-permeability, pulmonary edema, pulmonary hypertension and neutrophilic sequestration. AZA attenuated IR-induced lung injury, associated with decreases in carbonic anhydrase expression and pCO2 levels, as well as restoration of Na-K-ATPase expression.

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Propofol attenuates oxidant-induced acute lung injury in an isolated perfused rabbit-lung model

Abstract: Propofol attenuates oxidant-induced ALI in an isolated perfused rabbit lung model, probably due to its antioxidant action.

Cited by 12 publications

References 21 publications

Propofol Prevents Lung Injury Following Intestinal Ischemia-Reperfusion

Propofol Prevents Lung Injury Following Intestinal Ischemia-Reperfusion

Dose‐dependent protective effect of propofol against mitochondrial dysfunction in ischaemic/reperfused rat heart: role of cardiolipin

Carbonic anhydrase inhibitor attenuates ischemia-reperfusion induced acute lung injury

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