Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem Observations
Background. Myocardial depression in sepsis is common, and it is associated with higher mortality. In recent years, the hypothesis that the myocardial dysfunction during sepsis could be mediated by ischemia related to decreased coronary blood flow waned and a complex mechanism was invoked to explain...
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2016/3423450 |
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| author | M. Neri I. Riezzo C. Pomara S. Schiavone E. Turillazzi |
| author_facet | M. Neri I. Riezzo C. Pomara S. Schiavone E. Turillazzi |
| author_sort | M. Neri |
| collection | DOAJ |
| description | Background. Myocardial depression in sepsis is common, and it is associated with higher mortality. In recent years, the hypothesis that the myocardial dysfunction during sepsis could be mediated by ischemia related to decreased coronary blood flow waned and a complex mechanism was invoked to explain cardiac dysfunction in sepsis. Oxidative stress unbalance is thought to play a critical role in the pathogenesis of cardiac impairment in septic patients. Aim. In this paper, we review the current literature regarding the pathophysiology of cardiac dysfunction in sepsis, focusing on the possible role of oxidative-nitrosative stress unbalance and mitochondria dysfunction. We discuss these mechanisms within the broad scenario of cardiac involvement in sepsis. Conclusions. Findings from the current literature broaden our understanding of the role of oxidative and nitrosative stress unbalance in the pathophysiology of cardiac dysfunction in sepsis, thus contributing to the establishment of a relationship between these settings and the occurrence of oxidative stress. The complex pathogenesis of septic cardiac failure may explain why, despite the therapeutic strategies, sepsis remains a big clinical challenge for effectively managing the disease to minimize mortality, leading to consideration of the potential therapeutic effects of antioxidant agents. |
| format | Article |
| id | doaj-art-4b7e4ee2158c4f13b20207e258ab34b4 |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-4b7e4ee2158c4f13b20207e258ab34b42025-08-20T02:38:35ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/34234503423450Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem ObservationsM. Neri0I. Riezzo1C. Pomara2S. Schiavone3E. Turillazzi4Institute of Forensic Pathology, Department of Clinical and Experimental Medicine, University of Foggia, Ospedale Colonnello D’Avanzo, Viale degli Aviatori 1, 71100 Foggia, ItalyInstitute of Forensic Pathology, Department of Clinical and Experimental Medicine, University of Foggia, Ospedale Colonnello D’Avanzo, Viale degli Aviatori 1, 71100 Foggia, ItalyInstitute of Forensic Pathology, Department of Clinical and Experimental Medicine, University of Foggia, Ospedale Colonnello D’Avanzo, Viale degli Aviatori 1, 71100 Foggia, ItalyInstitute of Pharmacology, Department of Clinical and Experimental Medicine, University of Foggia, Via L. Pinto 1, 71100 Foggia, ItalyInstitute of Forensic Pathology, Department of Clinical and Experimental Medicine, University of Foggia, Ospedale Colonnello D’Avanzo, Viale degli Aviatori 1, 71100 Foggia, ItalyBackground. Myocardial depression in sepsis is common, and it is associated with higher mortality. In recent years, the hypothesis that the myocardial dysfunction during sepsis could be mediated by ischemia related to decreased coronary blood flow waned and a complex mechanism was invoked to explain cardiac dysfunction in sepsis. Oxidative stress unbalance is thought to play a critical role in the pathogenesis of cardiac impairment in septic patients. Aim. In this paper, we review the current literature regarding the pathophysiology of cardiac dysfunction in sepsis, focusing on the possible role of oxidative-nitrosative stress unbalance and mitochondria dysfunction. We discuss these mechanisms within the broad scenario of cardiac involvement in sepsis. Conclusions. Findings from the current literature broaden our understanding of the role of oxidative and nitrosative stress unbalance in the pathophysiology of cardiac dysfunction in sepsis, thus contributing to the establishment of a relationship between these settings and the occurrence of oxidative stress. The complex pathogenesis of septic cardiac failure may explain why, despite the therapeutic strategies, sepsis remains a big clinical challenge for effectively managing the disease to minimize mortality, leading to consideration of the potential therapeutic effects of antioxidant agents.http://dx.doi.org/10.1155/2016/3423450 |
| spellingShingle | M. Neri I. Riezzo C. Pomara S. Schiavone E. Turillazzi Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem Observations Mediators of Inflammation |
| title | Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem Observations |
| title_full | Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem Observations |
| title_fullStr | Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem Observations |
| title_full_unstemmed | Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem Observations |
| title_short | Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem Observations |
| title_sort | oxidative nitrosative stress and myocardial dysfunctions in sepsis evidence from the literature and postmortem observations |
| url | http://dx.doi.org/10.1155/2016/3423450 |
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