Low tidal volume protects pulmonary vasomotor function from “second-hit” injury in acute lung injury rats

Pan, Chun; Wang, Jianqiang; Liu, Wei; Liu, Ling; Liang, Jing; Yang, Yi; Qiu, Haibo

doi:10.1186/1465-9921-13-77

Cited by 23 publications

(21 citation statements)

References 29 publications

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“…Previous studies reported that levels of circulatory and pulmonary ET-1 are elevated in ARDS models [16,21,22]. The current data are consistent with data from these earlier reports.…”

Section: Discussionsupporting

confidence: 92%

“…Thus, collectively, data from the present study and these earlier studies show a significant alteration in levels of both circulatory and pulmonary ET-1 compared to the healthy control subjects in lavage-induced surfactant depleted ARDS models. Secondly, these data suggest validation of the present animal model as a suitable model for ARDS, including the patterns of circulatory and pulmonary ET-1 levels as seen in other frequently used ARDS models [16,21,22].…”

Section: Discussionmentioning

confidence: 77%

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Effects of Closed Vs. Open Repeated Endotracheal Suctioning During Mechanical Ventilation on the Pulmonary and Circulatory Levels of Endothelin-1 in Lavage-Induced Rabbit ARDS Model

Sakuramoto¹,

Jesmin²,

Shimojo³

et al. 2014

J Vasc Med Surg

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Background: A growing body of evidence demonstrates discretely the difference of open endotracheal suctioning (OES) and closed endotracheal suctioning (CES) on the respiratory and hemodynamic parameters in acute respiratory distress syndrome (ARDS). Endothelin-1 (ET-1), a mediator of vascular inflammation, cell proliferation, and fibrosis in addition to being a potent vasoconstrictor has been potentially implicated in the pathogenesis of ARDS. Here, we investigated the effects of repeated OES vs. CES during mechanical ventilation on circulatory and pulmonary levels of ET-1 in ARDS. Methods: Briefly, 22 Japanese White Rabbits were intubated with a 3.5-mm endotracheal tube. Normal saline was instilled into lung and washed mildly. After instillation, rabbits were ventilated at definite setting; OES and CES duration was for 6 hours and performed every 30 minutes from protocol start. Results: At circulatory level, either OES or CES did not alter plasma ET-1 level compared to the ET-1 level in ARDS before the initiation of endotracheal suctioning (OES 4.7 ± 1.3 pg/ml vs. CES 4.8 ± 1.5 pg/ml, p=0.839). In contrast, pulmonary ET-1 level was significantly higher in CES group compared to OES group after 6 hours of repeated suctioning in ARDS (OES 26.9 ± 2.2 pg/mg vs. CES 29.9 ± 3.3 pg/mg, p=0.018). This change in pulmonary ET-1 level could maintain a parallel relation with PaO 2 level. Conclusion: At this moment, we can not clarify the mechanism and effects of the observed change in ET-1 in a rabbit model of ARDS as well as its clinical impact.

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“…Previous studies reported that levels of circulatory and pulmonary ET-1 are elevated in ARDS models [16,21,22]. The current data are consistent with data from these earlier reports.…”

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 77%

Effects of Closed Vs. Open Repeated Endotracheal Suctioning During Mechanical Ventilation on the Pulmonary and Circulatory Levels of Endothelin-1 in Lavage-Induced Rabbit ARDS Model

Sakuramoto¹,

Jesmin²,

Shimojo³

et al. 2014

J Vasc Med Surg

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“…Both iNOS and endothelin-1 have been associated with astrocyte dysfunction in several neurological conditions, including brain ischemia [19,20]. A recent study in rats further con rmed the association between tidal volume, endothelin-1 and NO synthetase [21]. Thus, one hypothesis to account for our results could be formulated as follows: low tidal volume ventilation, perhaps coupled with the effects of a higher respiratory rate, leads to increased endothelin levels and induced NO synthetase.…”

Section: Discussionsupporting

confidence: 67%

Lung-Protective Ventilation Increases Cerebral Metabolism and Non-Inflammatory Brain Injury in Porcine Experimental Sepsis

Nyberg

Gremo

Blixt

et al. 2020

Preprint

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Background: Protective ventilation with lower tidal volumes reduces systemic and organ-specific inflammation. In sepsis-induced encephalopathy or acute brain injury the use of protective ventilation has not been widely investigated (experimentally or clinically). We hypothesized that protective ventilation would attenuate cerebral inflammation in a porcine endotoxemic sepsis model. The aim of the study was to study the effect of tidal volume on cerebral inflammatory response, cerebral metabolism and brain injury. Nine animals received protective mechanical ventilation with a tidal volume of 6 mL x kg-1 and nine animals were ventilated with a tidal volume of 10 mL x kg-1. During a 6-hour experiment, the pigs received an endotoxin intravenous infusion of 0.25 µg x kg-1 x h-1. Systemic, superior sagittal sinus and jugular vein blood samples were analysed for inflammatory cytokines and S100B. Intracranial pressure, brain tissue oxygenation and brain microdialysis were sampled every hour. Results: No differences in systemic or sagittal sinus levels of TNF-α or IL-6 were seen between the groups. The low tidal volume group had increased cerebral blood flow (p<0.001) and cerebral oxygen delivery (p<0.001), lower cerebral vascular resistance (p<0.05), higher cerebral metabolic rate (p<0.05) along with higher cerebral glucose consumption (p<0.05) and lactate production (p<0.05). Moreover, low tidal volume ventilation increased the levels of glutamate (p<0.01), glycerol (p<0.08) and showed a trend towards higher lactate to pyruvate ratio (p=0.08) in cerebral microdialysate as well as higher levels of S-100B (p<0.05) in jugular venous plasma compared with medium-high tidal volume ventilation.Conclusions: Contrary to the hypothesis, protective ventilation did not affect inflammatory cytokines. The low tidal volume group had increased cerebral blood flow, cerebral oxygen delivery and cerebral metabolism together with increased levels of markers of brain injury compared with medium-high tidal volume ventilation.

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“…Zhang et al (2010) reported that pulmonary arteries of LPStreated rats have an increase in the contractile response to PE. In addition, LPS-treated rabbits showed a decrease in both endothelium-dependent and -independent vasorelaxation (Huang et al 2005).Conversely, the relaxation response to SNP in PA rings of LPS-treated rats has been shown to be unaffected (Pan et al 2012). In this study, LPS-treated rats showed an increase in the contractile response of PA rings to PE without affecting either endothelium-dependent or -independent vasorelaxation.…”

Section: Activation Of Nf-κb Is Increased During Inflammation and It mentioning

confidence: 94%

LPS-RS attenuation of lipopolysaccharide-induced acute lung injury involves NF-κB inhibition

Abdelmageed

El‐Awady

Abdelrahim

et al. 2016

Can. J. Physiol. Pharmacol.

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In this study, we studied the effect of lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS), an inhibitor of Toll-like receptor 4 (TLR4), in LPS-induced acute lung injury (ALI). Male Sprague-Dawley rats were treated with LPS-RS (0.1 mg/kg body mass, by intraperitoneal (i.p.) injection) 1 h before LPS injection (10 mg/kg, i.p.). Bronchoalveolar lavage fluid (BALF) and lung tissues were collected 24 h later to determine total and differential cell count, total protein content, levels of lactate dehydrogenase (LDH), histopathological changes, markers of oxidative stress, and mRNA expression of the inhibitory protein nuclear factor kappaB-α (NFκBIA) and TLR4. Additionally, rings of pulmonary artery were isolated for measuring vascular reactivity. LPS-induced ALI was indicated by increases in total and differential cell count, total protein, and LDH in BALF, and increased lung levels of malondialdehyde (MDA), as well as decreased activity of reduced glutathione (GSH) and superoxide dismutase (SOD). Moreover, LPS increased pulmonary artery contraction in response to phenylephrine (PE). Additionally, LPS downregulated mRNA expression of NFκBIA and upregulated mRNA expression of TLR4. LPS caused a marked inflammation in the lung tissue, with tubercular granuloma and numerous neutrophils. Pretreatment with LPS-RS protected against LPS-induced ALI by decreasing total and differential cell count, total protein, and LDH in BALF, and increased pulmonary GSH content and SOD activity without affecting MDA content. Additionally, it decreased the elevated PE-induced pulmonary artery contraction. LPS-RS upregulated mRNA expression of NFκBIA and downregulated mRNA expression of TLR4. Moreover, LPS-RS prevented inflammation in lung tissues. In conclusion, pretreatment with LPS-RS protects against LPS-induced ALI in rats through its anti-inflammatory effects, possibly by decreasing the mRNA expression of TLR4 and increasing that of NFκBIA.

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Low tidal volume protects pulmonary vasomotor function from “second-hit” injury in acute lung injury rats

Cited by 23 publications

References 29 publications

Effects of Closed Vs. Open Repeated Endotracheal Suctioning During Mechanical Ventilation on the Pulmonary and Circulatory Levels of Endothelin-1 in Lavage-Induced Rabbit ARDS Model

Effects of Closed Vs. Open Repeated Endotracheal Suctioning During Mechanical Ventilation on the Pulmonary and Circulatory Levels of Endothelin-1 in Lavage-Induced Rabbit ARDS Model

Lung-Protective Ventilation Increases Cerebral Metabolism and Non-Inflammatory Brain Injury in Porcine Experimental Sepsis

LPS-RS attenuation of lipopolysaccharide-induced acute lung injury involves NF-κB inhibition

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