Inflammatory Consequences of Lung Ischemia-Reperfusion Injury and Low-Pressure Ventilation

Cobelens, Pieter M.; Putte, Bart P. van; Kavelaars, Annemieke; Heijnen, Cobi J.; Kesecioğlu, Jozef

doi:10.1016/j.jss.2008.04.022

Cited by 27 publications

(29 citation statements)

References 26 publications

(28 reference statements)

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“…Notably, Determann et al showed mechanical ventilation with lower tidal volumes also to attenuate development of lung injury in patients without ALI at the onset of mechanical ventilation (Determann et al, 2010). Recent research however, provided striking evidence that even "lung-protective" ventilator settings may result in the development of important aspects of VILI (Cobelens et al, 2009;Vaneker et al, 2007;Wolthuis et al, 2009b). We confirmed these prior reports in a murine model of VILI.…”

Section: Therapeutic Interventions In Critically Ill Patients With Vesupporting

confidence: 84%

Ventilator-Induced Lung Injury: Mechanisms and Future Therapeutic Interventions

Hegeman¹,

Schultz²,

Heijnen³

et al. 2012

Front Lines of Thoracic Surgery

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Section: Therapeutic Interventions In Critically Ill Patients With Vesupporting

confidence: 84%

Ventilator-Induced Lung Injury: Mechanisms and Future Therapeutic Interventions

Hegeman¹,

Schultz²,

Heijnen³

et al. 2012

Front Lines of Thoracic Surgery

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“…While necrosis may be one mechanism of myocardial death in SAP, it was found that myocardial cells undergo apoptosis under oxygen depletion and other detrimental conditions [19,20]. To determine whether myocardial apoptosis occurs in SAP rats and whether IMD has a protective effect on myocardial cells, we examined myocardial apoptosis using TUNEL staining.…”

Section: Administration Of Imd Reduced Myocardial Apoptosis In Sap Ratsmentioning

confidence: 99%

“…Hypoperfusion and oxygen depletion cause activation of the apoptotic cascade in cardiomyocytes [19]. To determine whether IMD administration influences the apoptotic cascade, we examined gene expression for the pro-survival factor Bcl-2, and the pro-apoptotic factor Bax (Fig.…”

Section: Imd Inhibits Myocardial Apoptosis Through Regulating Pro-andmentioning

confidence: 99%

Protective effect of intermedin on myocardial cell in a rat model of severe acute pancreatitis

Cao

Xue

et al. 2011

Cellular and Molecular Biology Letters

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Abstract:Severe acute pancreatitis (SAP) is a common disease with a poor prognosis. Heart failure is one cause of SAP patient death. Intermedin (IMD) is a potent endogenous cardio-protective substance. Administration of exogenous IMD showed beneficial effects in cardiovascular diseases. The aim of this study was to investigate the myocardial damage in SAP and to determine the therapeutic potential of IMD for SAP. Using an SAP rat model, we examined endogenous IMD expression following SAP induction, and determined the effect of IMD on myocardial function, histological morphology, apoptosis-related gene expression, and prognosis. Our results indicated that the cardiac function and histological structure were significantly disrupted in SAP rats. Infusion of exogenous IMD significantly preserved cardiac function and ameliorated myocardial damage. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) revealed that myocardial apoptosis was extensively present in SAP rats, and IMD infusion led to increased expression of the prosurvival factor Bcl-2, but decreased pro-apoptotic factors Bax and caspase-3. In addition, IMD infusion also reversed the change of IMD receptor systems in SAP rat heart tissue. Furthermore, we found that IMD infusion greatly decreased mortality of SAP rats. In conclusion, administration of SAP produced therapeutic effects in SAP through modulating apoptotic and pro-survival gene expression, inhibiting myocardial apoptosis, preserving cardiac function, and ultimately increasing survival. The current study suggests that IMD may be a useful therapeutic agent for SAP, and provides us an insight for a clinical trial of IMD for treating human severe acute pancreatitis.

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“…It is well known that OLV in itself, regardless of surgical manipulations, may induce inflammatory changes at the level of small airways and lung parenchyma, through diverse mechanisms [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22]. The latter include elevated positive pressure (barotrauma), alveolar overdistension (volutrauma) [8,10], repetitive collapse-reopening cycles (atelettrauma) [10], low oxygen tension, and the so-called reventilation injury [13,14,22].…”

Section: General Principlesmentioning

confidence: 99%

“…The latter include elevated positive pressure (barotrauma), alveolar overdistension (volutrauma) [8,10], repetitive collapse-reopening cycles (atelettrauma) [10], low oxygen tension, and the so-called reventilation injury [13,14,22]. All these factors are responsible for oxidative stress [16,19,20,21] and excess recruitment of inflammatory cells, with subsequent activation of cytokine network and establishment of an inflamed microenvironment [8,[11][12][13]15]. These compartmental changes, which can involve both the dependent and non-dependent (operated) lung, configure a condition known as "Ventilator-Associated Lung Injury" (VALI).…”

Section: General Principlesmentioning

confidence: 99%