Cardioprotective Effect of Aprotinin on Myocardial Ischemia/Reperfusion Injury During Cardiopulmonary Bypass

Karaca, Pelin; Konuralp, Cüneyt; Enç, Yavuz; Süzer, Asuman; Sokullu, Onur; Ayoglu, Umut; Çïçek, Sertaç

doi:10.1253/circj.70.1432

Cited by 16 publications

(9 citation statements)

References 30 publications

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“…It should be noted that we have no established biological marker in the blood for acute lung injury. Indeed, only LDH has been occasionally used for this purpose but it is highly nonspecific and characterised by slow kinetics [43,44]. Regardless we observed a weak correlation between greatest LDH and SPB changes.…”

Section: Discussionmentioning

confidence: 51%

Surfactant protein B and RAGE increases in the plasma during cardiopulmonary bypass: a pilot study

et al. 2010

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Surfactant derived protein B (SPB) and plasma receptor for advanced glycation end products (RAGE) have been proposed as markers of lung injury. The former is produced specifically by pneumocytes while RAGE production is present in several body tissues. Cardiopulmonary bypass (CPB) generates a transient lung injury. We measured SPB and RAGE in plasma before surgery and after CPB, as well as 24 h and 48 h later.We analysed plasma samples from 20 subjects scheduled for elective coronary artery bypass grafting. We performed a quantitative analysis of plasma levels of RAGE and SPB mature form (8 kDa) by ELISA and a semi-quantitative analysis of SPB immature form (,40 kDa) by Western blotting.Surgery procedures were uneventful. After CPB RAGE median (75th-25th interquartile difference) increased from 633 (539)

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Section: Discussionmentioning

confidence: 51%

Surfactant protein B and RAGE increases in the plasma during cardiopulmonary bypass: a pilot study

et al. 2010

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“…Karaca studied the expression alteration of lactate dehydrogenase gene, induced by ischemia-reperfusion. They previously proved that the expression of ldh gene rises in response to ischemia (Karaca et al, 2006;Xu et al, 2006), but at the same time our results have shown that in response to normoxic perfusion LDH was down- Hemodynamic parameters, like coronary flow and heart rate were also measured. None of these parameters changed in the perfused groups when compared to controls.…”

Section: Gene Expression Alteration Due To Perfusionsupporting

confidence: 54%

Gene and protein expression changes in response to normoxic perfusion in mouse hearts

Faragó

Kocsis

Feher

et al. 2008

Journal of Pharmacological and Toxicological Methods

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Introduction: Although crystalloid-perfused isolated heart models are widely used in cardiovascular research, there are several limitations of these techniques. Changes in cardiac gene expression pattern due to normoxic perfusion itself have not been studied, despite its potential importance to provide useful information on limitations of this model. Therefore, here we investigated the time-dependent effect of normoxic, normothermic perfusion on global gene expression at mRNA and protein levels. Methods: Hearts from male CFLP mice were perfused according to the Langendorff technique. We assessed relative gene expression changes by DNA microarray analysis of 8000 genes after 0, 60 and 120 min perfusion. Results: Twelve genes exhibited significant up-regulation and 27 showed repression in hearts perfused for 60 or 120 min as compared to 0 min controls. Expression changes of 17 selected genes were verified and an additional 19 genes were examined by real-time quantitative PCR. Genes with altered expression included those coding for Creatin kinase, Lactate dehydrogenase, Voltage-dependent anion channel 1, a Disintegrin and Metalloprotease domain 3, Integrin alpha 7, Long-chain acyl-CoA dehydrogenase, Casein kinase II, Ketohexokinase, Chloride ion current inducer protein, Matrix metalloproteinase 2 and 9, Superoxide dismutases and Nitric oxide synthases, etc. Discussion: Our results show that normoxic crystalloid perfusion itself results in time-dependent changes in cardiac gene expression which should be considered when designing ex vivo perfusion protocols in the mouse heart to mimic cardiac pathologies as many of these genes have been suspected to influence several cardiovascular diseases.

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“…Considering the high sensitivity, high specificity, and strong predictive value of cTnI for myocardial injury, cTnI could be a strong predictor for assessment of myocardial injury after CABG. Protective measures such as aprotinin, a serine protease inhibitor, can thus be administered accordingly, as demonstrated in a recent study 40 …”

Section: Discussionmentioning

confidence: 99%

Release of Cardiac Biochemical and Inflammatory Markers in Patients on Cardiopulmonary Bypass Undergoing Coronary Artery Bypass Grafting

Meng¹,

Zhu²,

Sohn³

et al. 2008

Journal of Cardiac Surgery

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Cardioprotective Effect of Aprotinin on Myocardial Ischemia/Reperfusion Injury During Cardiopulmonary Bypass

Cited by 16 publications

References 30 publications

Surfactant protein B and RAGE increases in the plasma during cardiopulmonary bypass: a pilot study

Surfactant protein B and RAGE increases in the plasma during cardiopulmonary bypass: a pilot study

Gene and protein expression changes in response to normoxic perfusion in mouse hearts

Release of Cardiac Biochemical and Inflammatory Markers in Patients on Cardiopulmonary Bypass Undergoing Coronary Artery Bypass Grafting

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