Добірка наукової літератури з теми "Myocardial ischaemic-reperfusion injury"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Зміст
Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Myocardial ischaemic-reperfusion injury".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Статті в журналах з теми "Myocardial ischaemic-reperfusion injury"
1
Hausenloy, Derek. "Signalling pathways in ischaemic postconditioning." Thrombosis and Haemostasis 101, no. 04 (2009): 626–34. http://dx.doi.org/10.1160/th08-11-0734.
Повний текст джерелаАнотація:
SummaryCoronary heart disease (CHD) is the leading cause of death globally. Following an acute coronary artery occlusion, timely myocardial reperfusion using either primary percutaneous coronary intervention (PCI) or thrombolytic therapy remains the most effective treatment strategy for reducing myocardial infarct size, preventing left ventricular remodelling, preserving left ventricular systolic function and improving clinical outcomes. However, the full benefits of myocardial reperfusion are not realised, given that the actual process of reperfusing ischaemic myocardium can independently induce cell death – a phenomenon termed lethal reperfusion injury. Ischaemic postconditioning represents an innovative treatment strategy for limiting lethal myocardial reperfusion injury and further reducing myocardial infarct size for those patients undergoing primary PCI. It is achieved by interrupting the normal myocardial reperfusion process, with several intermittent episodes of coronary myocardial ischaemia induced by low-pressure inflations of the angioplasty balloon in the infarct-related coronary artery. Experimental studies demonstrate that this stuttered form of myocardial reperfusion improves myocardial perfusion, maintains endothelial function, attenuates apoptotic cell death, reduces myocardial infarct size, preserves left ventricular systolic function and reduces mortality. The mechanisms underlying the cardioprotective effect of ischaemic postconditioning are the subject of intense investigation. In this article we review the signalling pathways which have been implicated as potential mediators of ischaemic postconditioning, the identification of which have provided novel pharmacological targets of cardioprotection capable of recapitulating the protective benefits of ischaemic postconditioning.
2
Saeid, Feyzizadeh, Javadi Aniseh, Badalzadeh Reza, and Vafaee S. Manouchehr. "Signaling mediators modulated by cardioprotective interventions in healthy and diabetic myocardium with ischaemia–reperfusion injury." European Journal of Preventive Cardiology 25, no. 14 (February 14, 2018): 1463–81. http://dx.doi.org/10.1177/2047487318756420.
Повний текст джерелаАнотація:
Ischaemic heart diseases are one of the major causes of death in the world. In most patients, ischaemic heart disease is coincident with other risk factors such as diabetes. Patients with diabetes are more prone to cardiac ischaemic dysfunctions including ischaemia–reperfusion injury. Ischaemic preconditioning, postconditioning and remote conditionings are reliable interventions to protect the myocardium against ischaemia–reperfusion injuries through activating various signaling pathways and intracellular mediators. Diabetes can disrupt the intracellular signaling cascades involved in these myocardial protections, and studies have revealed that cardioprotective effects of the conditioning interventions are diminished in the diabetic condition. The complex pathophysiology and poor prognosis of ischaemic heart disease among people with diabetes necessitate the investigation of the interaction of diabetes with ischaemia–reperfusion injury and cardioprotective mechanisms. Reducing the outcomes of ischaemia–reperfusion injury using targeted strategies would be particularly helpful in this population. In this study, we review the protective interventional signaling pathways and mediators which are activated by ischaemic conditioning strategies in healthy and diabetic myocardium with ischaemia–reperfusion injury.
3
Churchill, E. N., та D. Mochly-Rosen. "The roles of PKCδ and ϵ isoenzymes in the regulation of myocardial ischaemia/reperfusion injury". Biochemical Society Transactions 35, № 5 (25 жовтня 2007): 1040–42. http://dx.doi.org/10.1042/bst0351040.
Повний текст джерелаАнотація:
Reperfusion of ischaemic cardiac tissue is associated with increased apoptosis and oncosis, resulting in diminished heart function. Short bouts of ischaemia before the prolonged ischaemic event (ischaemic preconditioning) protect the heart from injury mediated by reperfusion. The PKC (protein kinase C) family of serine/threonine kinases are involved in many different signalling processes. Two calcium-insensitive isoforms of the novel PKC subfamily, PKCδ and ϵ, play opposing roles in ischaemia/reperfusion injury. Activation of PKCδ during reperfusion induces cell death through the regulation of mitochondrial function and induction of apoptosis and oncosis. In contrast, activation of PKCϵ before ischaemia protects mitochondrial function and diminishes apoptosis and oncosis. How can two highly homologous PKC isoenzymes play such opposing roles through the regulation of mitochondrial function? This review will highlight what is known about PKCδ and ϵ function during ischaemia/reperfusion injury and will suggest a novel regulatory pathway which determines the fate of the cell following ischaemic stress.
4
Wagner, Robert, Pavel Piler, Zufar Gabbasov, Junko Maruyama, Kazuo Maruyama, Jiri Nicovsky, and Peter Kruzliak. "Adjuvant Cardioprotection in Cardiac Surgery: Update." BioMed Research International 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/808096.
Повний текст джерелаАнотація:
Cardiac surgery patients are now more risky in terms of age, comorbidities, and the need for complex procedures. It brings about reperfusion injury, which leads to dysfunction and/or loss of part of the myocardium. These groups of patients have a higher incidence of postoperative complications and mortality. One way of augmenting intraoperative myocardial protection is the phenomenon of myocardial conditioning, elicited with brief nonlethal episodes of ischaemia-reperfusion. In addition, drugs are being tested that mimic ischaemic conditioning. Such cardioprotective techniques are mainly focused on reperfusion injury, a complex response of the organism to the restoration of coronary blood flow in ischaemic tissue, which can lead to cell death. Extensive research over the last three decades has revealed the basic mechanisms of reperfusion injury and myocardial conditioning, suggesting its therapeutic potential. But despite the enormous efforts that have been expended in preclinical studies, almost all cardioprotective therapies have failed in the third phase of clinical trials. One reason is that evolutionary young cellular mechanisms of protection against oxygen handling are not very robust. Ischaemic conditioning, which is among these, is also limited by this. At present, the prevailing belief is that such options of treatment exist, but their full employment will not occur until subquestions and methodological issues with the transfer into clinical practice have been resolved.
5
Rőth, Erzsébet. "A szabad gyökös reakciók jelentősége a szívizom ischaemiás-reperfúziós károsodásában és az endogén adaptáció indukálásában." Orvosi Hetilap 156, no. 47 (November 2015): 1908–11. http://dx.doi.org/10.1556/650.2015.30304.
Повний текст джерелаАнотація:
The reperfusion of acute ischaemic myocardium is essential for myocardial salvage, so called “gold standard” therapy, however it can results serious damage in the myocardium. Functional alterations occur, including depressed contractile function and decreased coronary flow as well as altered vascular reactivity. Over the several decades it has been demonstrated that oxygen radical formation is greatly increased in post-ischaemic heart and serves as a critical central mechanism of ischaemic-reperfusion injury. However it has been demonstrated that free radical play an important role in the endogenous adaptation phenomenon of the heart, too. Ischaemic preconditioning is a cellular adaptive response of the heart to stress, which provides the most potent endogenous protection against reperfusion arrhytmias, stunning and infarction. Postconditioning defined as brief periods of ischaemia and reperfusion during the very early minutes of reperfusion stimulates endogenous adaptation. Postconditioning may also attenuate the damage to endothelial cells and cardiomyocytes from oxidants, cytokines, proteases and inflammatory cells. Orv. Hetil., 2015, 156(47), 1908–1911.
6
Zarro, Debra L., David A. Palanzo, and Farrokh S. Sadr. "Myocardial preconditioning using adenosine: review and clinical experience." Perfusion 13, no. 2 (March 1998): 145–50. http://dx.doi.org/10.1177/026765919801300201.
Повний текст джерелаАнотація:
Adenosine is an endogenous nucleotide and a breakdown product of adenosine triphosphate. Adenosine has been proposed as a mediator of the ischaemic preconditioning phenomenon. Ischaemic reperfusion injury incurred during and following cardiopulmonary bypass contributes to depressed myocardial function after cardiac surgery. It is believed that administering adenosine via the aortic root, immediately following aortic crossclamping as well as just prior to removal of the aortic crossclamp, provides myocardial preconditioning resulting in improved cardiac protection during ischaemic arrest and retarding ischaemic reperfusion injury. A retrospective analysis was done utilizing consecutive patients undergoing coronary artery bypass grafting performed by the same surgeon. Some of the patients received myocardial preconditioning with adenosine. A comparison was made in postoperative cardiac function between patients who underwent myocardial preconditioning and those who did not receive adenosine. Results demonstrate a greater improvement in postoperative cardiac function, when compared to preoperative values, in those patients receiving myocardial preconditioning with adenosine.
7
Steffens, Sabine, Fabrizio Montecucco, and François Mach. "The inflammatory response as a target to reduce myocardial ischaemia and reperfusion injury." Thrombosis and Haemostasis 102, no. 08 (2009): 240–47. http://dx.doi.org/10.1160/th08-12-0837.
Повний текст джерелаАнотація:
SummaryAcute myocardial infarction is the leading cause of morbidity and mortality in the adult population of developed and developing nations. Although the prompt restoration of antegrade blood flow in the infarct-related coronary artery is the mean therapy for improving survival, reperfusion itself may cause damage to ischaemic myocardial tissue. This event is well known as “reperfusion injury”. Crucial mediators for cardiac damage in the reperfusion phases are oxidative stress, inflammation and leukocyte infiltration. Already approved and novel therapies might directly reduce these inflammatory processes. Treatments modulating chemokine secretion and activity should be considered as very promising approaches to reduce myocardial reperfusion injury.
8
Simonovic, Nina, and Jovana Jeremic. "Role of Calcium Channel Blockers in Myocardial Preconditioning." Serbian Journal of Experimental and Clinical Research 18, no. 4 (December 1, 2017): 281–87. http://dx.doi.org/10.1515/sjecr-2016-0073.
Повний текст джерелаАнотація:
AbstractCoronary heart disease is the leading cause of mortality and morbidity worldwide. The effects of coronary heart disease are usually attributable to the detrimental effects of acute myocardial ischaemia-reperfusion injury. Newer strategies such as ischaemic or pharmacological preconditioning have been shown to condition the myocardium to ischaemia-reperfusion injury and thus reduce the final infarct size. This review investigates the role of calcium channel blockers in myocardial preconditioning. Additionally, special attention is given to nicorandil whose mechanism of action may be associated with the cardioprotective effects of preconditioning. There are still many uncertainties in understanding the role of these agents in preconditioning, but future research in this direction will certainly help reduce coronary heart disease.
9
Yang, Yongjian, Yi Yang, Xiong Wang, Jin Du, Juanni Hou, Juan Feng, Yue Tian, Lei He, Xiuchuan Li, and Haifeng Pei. "Does growth differentiation factor 11 protect against myocardial ischaemia/reperfusion injury? A hypothesis." Journal of International Medical Research 45, no. 6 (August 25, 2016): 1629–35. http://dx.doi.org/10.1177/0300060516658984.
Повний текст джерелаАнотація:
The pathogenesis of myocardial ischaemia/reperfusion injury is multifactorial. Understanding the mechanisms of myocardial ischaemia/reperfusion will benefit patients with ischaemic heart disease. Growth differentiation factor 11 (GDF11), a member of the secreted transforming growth factor-β superfamily, has been found to reverse age-related hypertrophy, revealing the important role of GDF11 in cardiovascular disease. However, the functions of GDF11 in myocardial ischaemia/reperfusion have not been elucidated yet. A number of signalling molecules are known to occur downstream of GDF11, including mothers against decapentaplegic homolog 3 (SMAD3) and forkhead box O3a (FOXO3a). A hypothesis is presented that GDF11 has protective effects in acute myocardial ischaemia/reperfusion injury through suppression of oxidative stress, prevention of calcium ion overload and promotion of the elimination of abnormal mitochondria via both canonical (SMAD3) and non-canonical (FOXO3a) pathways. Since circulating GDF11 may mainly derive from the spleen, the lack of a spleen may make the myocardium susceptible to damaging insults. Administration of GDF11 may be an efficacious therapy to protect against cardiovascular diseases in splenectomized patients.
10
Chorawala, Mehul, Prem Prakash, Prakash Doddapattar, Manish Jain, Nirav Dhanesha, and Anil Chauhan. "Deletion of Extra Domain A of Fibronectin Reduces Acute Myocardial Ischaemia/Reperfusion Injury in Hyperlipidaemic Mice by Limiting Thrombo-Inflammation." Thrombosis and Haemostasis 118, no. 08 (June 30, 2018): 1450–60. http://dx.doi.org/10.1055/s-0038-1661353.
Повний текст джерелаАнотація:
Background Fibronectin splicing variant containing extra domain A (Fn-EDA), which is an endogenous ligand for Toll-like receptor 4 (TLR4), is present in negligible amounts in the plasma of healthy humans, but markedly elevated in patients with co-morbid conditions including diabetes and hyperlipidaemia, which are risk factors for myocardial infarction (MI). Very little is known about the role of Fn-EDA in the pathophysiology of acute MI under these co-morbid conditions. Materials and Methods We determined the role of Fn-EDA in myocardial ischaemia/reperfusion (I/R) injury in the hyperlipidaemic apolipoprotein E-deficient (ApoE−/−) mice. Infarct size, plasma cardiac troponin I (cTnI) levels, intravascular thrombosis (CD41-positive), neutrophil infiltration (Ly6 B.2-positive), neutrophil extracellular traps (citrullinated H3-positive) and myocyte apoptosis (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling-positive) were assessed in myocardial I/R injury model (1-hour ischaemia/23 hours of reperfusion). Results Irrespective of gender, Fn-EDA−/−ApoE−/− mice exhibited smaller infarct size and decreased cTnI levels concomitant with reduced post-ischaemic intra-vascular thrombi, neutrophils influx, neutrophil extracellular traps and myocyte apoptosis (p < 0.05 vs. ApoE−/− mice). Genetic deletion of TLR4 attenuated myocardial I/R injury in ApoE−/− mice (p < 0.05 vs. ApoE−/− mice), but did not further reduce in Fn-EDA−/− ApoE−/− mice suggesting that Fn-EDA requires TLR4 to mediate myocardial I/R injury. Bone marrow transplantation experiments revealed that Fn-EDA exacerbates myocardial I/R injury through TLR4 expressed on the haematopoietic cells. Infusion of a specific inhibitor of Fn-EDA, 15 minutes post-reperfusion, into ApoE−/− mice attenuated myocardial I/R injury. Conclusion Fn-EDA exacerbates TLR4-dependent myocardial I/R injury by promoting post-ischaemic thrombo-inflammatory response. Targeting Fn-EDA may reduce cardiac damage following coronary artery re-canalization after acute MI.
Дисертації з теми "Myocardial ischaemic-reperfusion injury"
1
Edroos, Sadat Ali. "Myocardial ischaemia-reperfusion injury and its reduction by remote ischaemic preconditioning in health and diabetes mellitus." Thesis, University of Leicester, 2014. http://hdl.handle.net/2381/31983.
Повний текст джерелаАнотація:
Myocardial infarction is the main cause of death in the United Kingdom. Early reperfusion of coronary artery occlusion has greatly improved mortality, though restoration of blood supply may perpetuate cell death through reperfusion injury. Preconditioning is a potent endogenous form of cardioprotection triggered through preceding brief nonperfusion of the heart’s blood supply. In remote conditioning it is triggered by intermittent tourniquet ischaemia of a limb. However a limited understanding of the mechanisms underlying transfer of a signal from the peripheries, its reception in the heart, and the impact of comorbid disease on this process hinders its application to the clinical setting of myocardial infarction. This work trials several models of reperfusion injury, and optimises a method of centrifugation of adult rat ventricular myocytes into a dense pellet to induce ischaemia, and simulate reperfusion by its dispersal. Remote preconditioning is evoked by preincubation of myocytes with serum samples taken from participants. This is used as a screening tool in order to test serum samples acquired from volunteers in control and disease states undergoing tourniquet ischaemia of a peripheral limb to reproduce the stimulus of remote preconditioning. A protective signal was seen in serum taken from healthy subjects following remote preconditioning versus baseline serum (20.5±3.3 vs 37.2±4.5 % necrosis respectively, n = 21, p < 0.001). Protection is absent in diabetes mellitus type 1 (51.5±4.6% necrosis, n = 14) and type 2 (51.3±8.2% necrosis, n = 10). The protective signal is preserved with age in healthy male participants, though appears to decline with age in a preliminary cohort of female participants. On assay of putative mechanisms of remote preconditioning, serum nitrite did not change with preconditioning in healthy volunteers, though it was found to significantly decrease in diabetes mellitus type 1. The implications for the application of this powerful yet elusive form of innate cardiac protection are considered.
2
Yu, Che-kwan. "Remifentanil induces delayed cardioprotection in the rat against ischaemic and reperfusion injury via Kappa, delta, mu opioid receptors and inducible heat shock protein 70." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634395.
Повний текст джерела
3
Yu, Che-kwan, and 俞治均. "Remifentanil induces delayed cardioprotection in the rat against ischaemic and reperfusion injury via Kappa, delta, mu opioid receptorsand inducible heat shock protein 70." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634395.
Повний текст джерела
4
Tsang, Sharon. "Role of testosterone and its interaction with adrenoceptor in protection against ischaemic insult and contractile function of the heart." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290732.
Повний текст джерела
5
Tsang, Sharon, and 曾舒蘭. "Role of testosterone and its interaction with adrenoceptor in protection against ischaemic insult and contractile function of theheart." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290732.
Повний текст джерела
6
Lee, Samuel Man. "Investigating the role of toll-like receptor 4 in myocardial ischaemic-preconditioning and ischaemic-reperfusion injury." Thesis, 2018. http://hdl.handle.net/2440/113614.
Повний текст джерелаАнотація:
Ischaemic heart disease remains a significant cause of death throughout the developed world.
Although technological advancements and improved health care have significantly reduced
mortality rates in the last century, additional research is required. Recently myocardial
inflammation has drawn increasing interest as a potential therapeutic against cardiovascular
disease. Because inflammation is activated by a broad range of pro-inflammatory mediators,
the innate immune response can be suppressed at multiple locations. Currently, most antiinflammatory
agents in phase III trials target specific pro-inflammatory cytokines such as TNF-
α, IL-1β and IL-6. These mediators have various roles ranging from the recruitment of white
blood cells to triggering cell death. In 2017 CANTOS (Canakinumab Anti-inflammatory
Thrombosis Outcomes Study), which investigated the therapeutic benefits of Canakinumab
(an IL-1β antagonist) in the cardiovascular setting, was completed. Although the study
reported that patients had a reduced risk of inheriting cardiovascular diseases, Canakinumab
did not reduce mortality rates. Considering the large number of inflammatory mediators
involved in myocardial ischaemic-reperfusion injury, blockade of a single cytokine may be
insufficient within the clinical setting. To date, no study has investigated whether the
suppression of upstream inflammatory receptors is more effective in attenuating myocardial
inflammation during ischaemic-reperfusion injury. This thesis investigates the role of toll-like
receptor 4 (TLR4), an immunosurveillance receptor, in both myocardial ischaemic-reperfusion
injury and ischaemic-preconditioning. Receptor activity is triggered when DAMPs (danger
associated molecular pattern molecules) are released from necrotic cells and bind onto the
TLR4 receptor complex. Evidence in the last two decades suggests that TLR4 can either exacerbate ischaemicreperfusion
injury or trigger a preconditioning response under certain conditions. Genetic or
pharmacological blockade of TLR4 has been reported limit infarct size, improve survival rates,
and suppress myocardial inflammation in in-vivo infarct animal studies. On the other hand,
evidence also suggests that low levels of TLR4 ligands can trigger preconditioning. In the
1990s, studies showed that pretreating animals with lipopolysaccharide, a bacterial ligand
recognised by TLR4, could protect animals against ischaemic-reperfusion injury. Additionally,
evidence also suggests that DAMPs can also elicit a preconditioning response when
administered prior ischaemia. Considering these findings TLR4 signalling may be regulated in
a biphasic manner which is dependent on the degree of TLR4 stimulation and the timing of
TLR4 activation.
Study 1 and 2 investigated whether the direct administration of a TLR4 antagonist during
ischaemic-preconditioning can influence contractile recovery after irreversible ischaemic
injury. The isolated heart technique was used to determine whether contractile function was
directly influenced by the blockade of TLR4. Study 3 and 4 examined if novel TLR4 antagonists
could protect against ischaemic-reperfusion injury in the in-vitro and in-vivo setting. To date,
no study has investigated whether the rapid administration of a TLR4 antagonist during
ischaemia can protect against myocardial ischaemic-reperfusion injury.
In brief, study 1 and 2’s results revealed that the suppression of TLR4 signalling in ischaemic-preconditioned
hearts depressed contractile recovery after ischaemic insult. Although protein
analyses revealed that cardiac fatty acid binding protein (cFABP) and high mobility group box one (HMGB1) were influenced by the suppression of TLR4 the data collected was conflicting.
Study 3 showed that (+)-naloxone and (+)-naltrexone suppressed LPS induced inflammation
but did not improve cell viability after simulated ischaemic-reperfusion injury. Finally (+)-
naloxone and TAK242 showed that both compounds could reduce myocardial infarct size and
inflammation in an in-vivo left anterior descending artery ligation model. The findings from
this thesis highlight the bivalent nature of TLR4 in ischaemic-preconditioning and ischaemicreperfusion
injury in both the acute and chronic setting.Thesis (Ph.D.) (Research by Publication) -- University of Adelaide, Adelaide Medical School, 2018
Книги з теми "Myocardial ischaemic-reperfusion injury"
1
Hausenloy, Derek, and Derek Yellon, eds. Novel Cardioprotective Strategies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0011.
Повний текст джерелаАнотація:
• Despite optimal therapy, the mortality and morbidity of coronary heart disease remains significant. Hence, novel treatment strategies of cardioprotection are required to improve clinical outcomes in these patients• Experimental studies have provided a plethora of therapeutic strategies for reducing myocardial injury, but the translation of these findings into the clinical setting has been largely disappointing. Many of these unsuccessful clinical studies have relied upon individually targeting established mediators of lethal reperfusion injury such as oxidative stress, inflammation, calcium overload and so forth• Clearly, novel targets for cardioprotection as well as a multi-targeted approach to cardioprotection directed against the multiple causes of lethal reperfusion injury are required to effect benefits in clinical outcomes• In this regard, the introduction of ischaemic postconditioning, a novel treatment strategy, in which following primary PCI the process of myocardial reperfusion is interrupted by several coronary re-occlusions, has been reported to reduce myocardial myocardial injury in AMI patients• Furthermore, experimental studies have identified the Reperfusion Injury Salvage Kinase (RISK) pathway and the mitochondrial permeability transition pore (mPTP) as novel targets for cardioprotection, which are currently been examined in the clinical setting.
2
Giacca, Mauro, and Borja Ibáñez. Advanced therapies to treat cardiovascular diseases: controversies and perspectives. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0028.
Повний текст джерелаАнотація:
There is a pressing need to develop novel therapies for myocardial infarction and heart failure, two conditions that affect over 20% of the world population. Despite important advances in achieving revascularization of the ischaemic myocardium and the usefulness of devices in assisting failing hearts, therapy for these conditions remains poor. The final extent of myocardial tissue loss after infarction is a major determinant of post-infarction mortality due to heart failure. In this chapter we review the current strategies aimed at counteracting injury due to acute myocardial ischaemia–reperfusion and the experimental approaches to achieve cardiac and vascular regeneration once damage has occurred. We critically discuss the possibility of inducing tissue restoration by gene transfer or exogenous cell implantation, and report on the exciting possibility of stimulating the endogenous capacity of cardiac regeneration using growth factors and small regulatory RNAs.
3
Pepper, John. Cardioprotection During Cardiac Surgery. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0007.
Повний текст джерелаАнотація:
• Overall early mortality for cardiac surgery is low at 2–3% but in high risk patients it can be high as 10–15%• The demography of cardiac surgical patients is changing to older and sicker patients• Myocardial ischaemia-reperfusion injury and the systemic inflammatory response are closely related• Several pharmacological agents that have been demon-strated to confer cardioprotection in the experimental setting have been applied to the clinical setting of cardiac surgery. However, the transfer of these findings from the bench to the bedside has been largely disappointing• Potential cardioprotective strategies include pharma-cological agents such as adenosine, and mechanical interventional strategies such as acute normovolaemic haemodilution and remote ischaemic preconditioning.