Myocardial membrane injury in pediatric cardiac surgery: An animal model

Egan, Jonathan R.; Butler, Tanya L.; Cole, Alexander J.; Abraham, Suresh K.; Murala, John Santosh Kumar; Baines, David; Street, Neil; Thompson, L. R.; Biecker, Oliver; Dittmer, John; Cooper, Sandra T.; Au, Carol G.; North, Klaus; Winlaw, David S.

doi:10.1016/j.jtcvs.2008.10.009

Cited by 8 publications

(9 citation statements)

References 26 publications

(54 reference statements)

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“…Among these enzymatic sources, much attention has been placed on xanthine oxidase in endothelial cells, NADPH oxidase in inflammatory cells and the mitochondrial electron transport chain reaction in cardiomyocytes using either in vivo models of ischemia-reperfusion or cultured endothelial cells and cardiomyocytes after hypoxia-reoxygenation [32, 45, 46]. It has been proposed that a burst of ROS from endothelial cells, and cardiomyocytes during early reperfusion can influence nearby neutrophils, setting up a local cycle of amplified cellular response through released inflammatory mediators.…”

Section: Role Of Ischemia-reperfusion In Myocardial Infarctionmentioning

confidence: 99%

Molecular Basis of Cardioprotective Effect of Antioxidant Vitamins in Myocardial Infarction

Rodrigo

Libuy

Feliú

et al. 2013

BioMed Research International

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Acute myocardial infarction (AMI) is the leading cause of mortality worldwide. Major advances in the treatment of acute coronary syndromes and myocardial infarction, using cardiologic interventions, such as thrombolysis or percutaneous coronary angioplasty (PCA) have improved the clinical outcome of patients. Nevertheless, as a consequence of these procedures, the ischemic zone is reperfused, giving rise to a lethal reperfusion event accompanied by increased production of reactive oxygen species (oxidative stress). These reactive species attack biomolecules such as lipids, DNA, and proteins enhancing the previously established tissue damage, as well as triggering cell death pathways. Studies on animal models of AMI suggest that lethal reperfusion accounts for up to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented. Although a number of strategies have been aimed at to ameliorate lethal reperfusion injury, up to date the beneficial effects in clinical settings have been disappointing. The use of antioxidant vitamins could be a suitable strategy with this purpose. In this review, we propose a systematic approach to the molecular basis of the cardioprotective effect of antioxidant vitamins in myocardial ischemia-reperfusion injury that could offer a novel therapeutic opportunity against this oxidative tissue damage.

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Section: Role Of Ischemia-reperfusion In Myocardial Infarctionmentioning

confidence: 99%

Molecular Basis of Cardioprotective Effect of Antioxidant Vitamins in Myocardial Infarction

Rodrigo

Libuy

Feliú

et al. 2013

BioMed Research International

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“…Animal models underwent 2 hours of cardiopulmonary bypass with or without pretreatment with PP188. PP188 was associated with potentially beneficial changes in membrane protein expression, reduced capillary leakage, less hemodilution [7], and reduced membrane injury from ischemia and reperfusion [8,11]. …”

Section: Discussionmentioning

confidence: 99%

“…Lipids are known to have no beneficial effects on myocardial protection from ischemia and reperfusion injury [28]. On the contrary, PP188 is known to have myocardial protective effects due to its cell membrane protecting effects [7-11]. However, the comparison between the MP group and the LP group revealed that hemodynamic parameters or infarct size were not significantly different between the two groups.…”

Section: Discussionmentioning

confidence: 99%

“…Poloxamer 188 (PP188) is nontoxic surface-active agent that has cytoprotective effects. PP188 is incorporated into the lipid bilayers, thereby decreasing their susceptibility to oxidative stress and inflammation [7-11]. Inhaled anesthetics, propofol, and PP188 provide cardioprotection against ischemia and reperfusion injury via different mechanisms [11], but despite these distinct mechanisms several studies have demonstrated that no additive or superior protection was observed with the combination of these cardioprotective agents [12,13].…”

Section: Introductionmentioning

confidence: 99%

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The cardioprotective effect of microemulsion propofol against ischemia and reperfusion injury in isolated rat heart

Hur

Kim

Lee

et al. 2012

Korean J Anesthesiol

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BackgroundLipid-emulsion propofol (LP) has cardioprotective effects against ischemia-reperfusion injury, but it has lipid-related side effects. Microemulsion propofol (MP) is a lipid-free propofol emulsified with 10% purified poloxamer 188 (PP188). PP188 is a nonionic surfactant and has cardioprotective effects. However, some reports have suggested that reduced cardioprotective effects were observed when the cardioprotective agents were used in combination even though each cardioprotective agent has cardioprotective effects. The aims of this study were to examine and compare the cardioprotective effects of MP and LP.Methods50 isolated rat hearts were perfused with modified Kreb's solution. They were divided into 4 groups and underwent 30 minutes of ischemia and 60 minutes of reperfusion. Control group: ischemia-reperfusion was performed without treatment. LP, MP and PP groups: LP, MP and PP188 were infused during the pre-ischemic and reperfusion period, respectively. Hemodynamic parameters and coronary effluent flow rate (CEFR) were measured. Infarct size was determined using triphenyl-tetrazolium staining.ResultsIn the MP group, systolic pressure was maintained near baseline, the systolic pressure was higher than that in the other groups and HR was lower than that in the other groups during reperfusion. Diastolic pressure was transiently increased in the PP group after treatment and at 5 minutes after reperfusion compared with that in the control group and in the the LP group. There were no differences in dP/dtmax and CEFR between groups. Infarct size in the LP, MP and PP groups was smaller than that in the control group, but there were no significant differences between these three groups.ConclusionsMP has cardioprotective effects similar to those of LP. MP can be used for cardiac anesthesia in cases with ischemia-reperfusion injury to avoid the lipid-related side effects of LP.

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“…Transcriptional regulation of AQPs is seen in the heart [53,82,83] and it is tempting to speculate that cardiac AQPs could be a therapeutic target to improve the outcome of ischaemic injury. Cardiac AQP4 expression has been reported to increase following focal ischaemia in the mouse [84].…”

Section: Physiological and Pathological Conditionsmentioning

confidence: 99%