Статті в журналах: "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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

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 джерела

Анотація:

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.

Стилі APA, Harvard, Vancouver, ISO та ін.

11

Fan, Qian, Xin-Chun Yang, Yu Liu, Le-Feng Wang, Sheng-Hui Liu, Yong-Gui Ge, Mu-Lie Chen, et al. "Postconditioning attenuates myocardial injury by reducing nitro-oxidative stress in vivo in rats and in humans." Clinical Science 120, no. 6 (December 3, 2010): 251–61. http://dx.doi.org/10.1042/cs20100369.

Повний текст джерела

Анотація:

In the present study, we hypothesized that postcon (postconditioning) confers cardioprotection in vivo by reducing the production of ONOO− (peroxynitrite) and nitro-oxidative stress subsequent to the inhibition of the iNOS (inducible NO synthase). Patients with AMI (acute myocardial infarct) were randomly assigned to undergo percutaneous coronary intervention without (control) or with ischaemic postcon by three episodes of 30-s inflation and 30-s deflation of the angioplasty balloon. Animal models of MI/R (myocardial ischaemia/reperfusion) injury were induced in rats by occluding the left coronary artery for 40 min followed by 4-h reperfusion. Rats were randomized to receive vehicle, postcon (three cycles of 10-s reperfusion and 10-s coronary re-occlusion preceding full reperfusion), the selective iNOS inhibitor 1400W or postcon plus 3-morpholinosydnonimine (an ONOO− donor). Postcon in patients reduced iNOS activity in white blood cells, decreased plasma nitrotyrosine, a fingerprint of ONOO− and an index of nitro-oxidative stress, and improved cardiac function (P<0.01 compared with control). In rats, postcon reduced post-ischaemic myocardial iNOS activity and nitrotyrosine formation, reduced myocardial infarct size (all P<0.05 compared with control) and improved cardiac function. Administration of 1400W resembled, whereas 3-morpholinosydnonimine abolished, the effects of postcon. In conclusion, reduction in ONOO−-induced nitro-oxidative stress subsequent to the inhibition of iNOS represents a major mechanism whereby postcon confers cardioprotection in vivo.

Стилі APA, Harvard, Vancouver, ISO та ін.

12

Muntean, Danina M., Adrian Sturza, Maria D. Dănilă, Claudia Borza, Oana M. Duicu, and Cristian Mornoș. "The Role of Mitochondrial Reactive Oxygen Species in Cardiovascular Injury and Protective Strategies." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–19. http://dx.doi.org/10.1155/2016/8254942.

Повний текст джерела

Анотація:

Ischaemia/reperfusion (I/R) injury of the heart represents a major health burden mainly associated with acute coronary syndromes. While timely coronary reperfusion has become the established routine therapy in patients with ST-elevation myocardial infarction, the restoration of blood flow into the previously ischaemic area is always accompanied by myocardial injury. The central mechanism involved in this phenomenon is represented by the excessive generation of reactive oxygen species (ROS). Besides their harmful role when highly generated during early reperfusion, minimal ROS formation during ischaemia and/or at reperfusion is critical for the redox signaling of cardioprotection. In the past decades, mitochondria have emerged as the major source of ROS as well as a critical target for cardioprotective strategies at reperfusion. Mitochondria dysfunction associated with I/R myocardial injury is further described and ultimately analyzed with respect to its role as source of both deleterious and beneficial ROS. Furthermore, the contribution of ROS in the highly investigated field of conditioning strategies is analyzed. In the end, the vascular sources of mitochondria-derived ROS are briefly reviewed.

Стилі APA, Harvard, Vancouver, ISO та ін.

13

Neckář, Jan, Adéla Boudíková, Petra Mandíková, Martin Štěrba, Olga Popelová, Ivan Mikšík, Ludmila Dabrowská, Jaroslav Mráz, Vladimír Geršl, and František Kolář. "Protective effects of dexrazoxane against acute ischaemia/reperfusion injury of rat hearts." Canadian Journal of Physiology and Pharmacology 90, no. 9 (September 2012): 1303–10. http://dx.doi.org/10.1139/y2012-096.

Повний текст джерела

Анотація:

Dexrazoxane (DEX), an inhibitor of topoisomerase II and intracellular iron chelator, is believed to reduce the formation of reactive oxygen species (ROS) and protects the heart from the toxicity of anthracycline antineoplastics. As ROS also play a role in the pathogenesis of cardiac ischaemia/reperfusion (I/R) injury, the aim was to find out whether DEX can improve cardiac ischaemic tolerance. DEX in a dose of 50, 150, or 450 mg·(kg body mass)–1 was administered intravenously to rats 60 min before ischaemia. Myocardial infarct size and ventricular arrhythmias were assessed in anaesthetized open-chest animals subjected to 20 min coronary artery occlusion and 3 h reperfusion. Arrhythmias induced by I/R were also assessed in isolated perfused hearts. Only the highest dose of DEX significantly reduced infarct size from 53.9% ± 4.7% of the area at risk in controls to 37.5% ± 4.3% without affecting the myocardial markers of oxidative stress. On the other hand, the significant protective effect against reperfusion arrhythmias occurred only in perfused hearts with the dose of DEX of 150 mg·kg–1, which also tended to limit the incidence of ischaemic arrhythmias. It is concluded that DEX in a narrow dose range can suppress arrhythmias in isolated hearts subjected to I/R, while a higher dose is needed to limit myocardial infarct size in open-chest rats.

Стилі APA, Harvard, Vancouver, ISO та ін.

14

Maulik, S. K., R. Kumari, M. Maulik, S. C. Manchanda, and S. K. Gupta. "Captopril and its time of administration in myocardial ischaemic-reperfusion injury." Pharmacological Research 44, no. 2 (August 2001): 123–28. http://dx.doi.org/10.1006/phrs.2001.0832.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

15

Liu, Hanqing, Wei Liu, Huiliang Qiu, Dezhi Zou, Huayang Cai, Qiuxiong Chen, Chaoyang Zheng, and Danping Xu. "Salvianolic acid B protects against myocardial ischaemia-reperfusion injury in rats via inhibiting high mobility group box 1 protein expression through the PI3K/Akt signalling pathway." Naunyn-Schmiedeberg's Archives of Pharmacology 393, no. 8 (December 18, 2019): 1527–39. http://dx.doi.org/10.1007/s00210-019-01755-7.

Повний текст джерела

Анотація:

AbstractSalvianolic acid B (Sal B) has a significant protective effect on myocardial ischaemia-reperfusion (I/R) injury. Therefore, the aims of this study were to determine the effects of Sal B on myocardial ischaemic-reperfusion (I/R) injury in rats and to explore whether its underlying mechanism of cardioprotection occurs through activating the expression of the phosphoinositide 3-kinase/protein, kinase B (PI3K/Akt) and inhibiting the expression of high mobility group protein 1 (HMGB1). Ninety Sprague-Dawley rats were randomized into five groups: group 1 (sham-operated), group 2 (myocardial I/R), group 3 (low dose of Sal B+I/R), group 4 (high dose of Sal B+I/R), and group 5 (high dose of Sal B+I/R+LY294002, which is a specific PI3k inhibitor). All I/R rats received 30 min myocardial ischaemia followed by 24-h reperfusion. Cardiac function, infarct size, myocardial injury marker levels, inflammatory response and cardiomyocyte apoptosis as well as Bcl-2, Bax, P-Akt, HMGB1 and TLR4 expression were measured. In the current study, Sal B significantly ameliorated myocardial I/R injury in a dose-dependent manner, ameliorated cardiac function, reduced myocardial infarction size, decreased myocardial injury marker expression, decreased inflammatory responses, reduced apoptosis, activated PI3K/Akt expression and inhibited HMGB1 expression. However, all effects of Sal B were significantly reversed by LY294002. Overall, the present study indicated that Sal B attenuated myocardial I/R injury by activating PI3K/Akt and inhibiting the release of HMGB1 in rats.

Стилі APA, Harvard, Vancouver, ISO та ін.

16

Han, Ya-Ling, Shao-Ha Li, Qin-Yue Zheng, Hong-Bin Wang, Guo-Yan Zhang, Zhong-Gui Wu, and Si-Cong Chen. "Changes and Relationship of PAF and TNF in Rats with Myocardial Ischaemia and Reperfusion Injury." Mediators of Inflammation 3, no. 3 (1994): 205–9. http://dx.doi.org/10.1155/s0962935194000281.

Повний текст джерела

Анотація:

In this study it is reported that: (1) the levels of blood platelet-activating factor and serum tumour necrosis factor significantly increased after coronary ligation and reperfusion, compared with sham-ligated controls, in an anaesthetized rat model; (2) compared with vehicle controls, pretreatment with the PAF antagonist BN 50739 (10 mg/kg, i.v.) produced significant decreases in infarct size (from 29.6 ± 4.0% to 22.4 ± 2.1%,p<0.05after 3 h ligation, and from 28.5 ± 9.5% to 10.5 ± 4.5%,p<0.01after 4 h reperfusion) and the level of serum TNF (from 10.4 ± 7.7 U/ml to 3.9 ± 4.8 U/ml,p<0.05); and (3) a significan positive correlation was found between the level of blood PAF or serum TNF and infarct size. The present results indicate that PAF and TNF may be important mediators involved in myocardial ischaemia and reperfusion injury, and that PAF antagonists may exert a protective effect on ischaemic or reperfused myocardium by inhibiting the interaction of PAF and TNF.

Стилі APA, Harvard, Vancouver, ISO та ін.

17

ZHANG, Jin-Gang, Sudip GHOSH, Colin D. OCKLEFORD, and Manuel GALIÑANES. "Characterization of an in vitro model for the study of the short and prolonged effects of myocardial ischaemia and reperfusion in man." Clinical Science 99, no. 5 (October 27, 2000): 443–53. http://dx.doi.org/10.1042/cs0990443.

Повний текст джерела

Анотація:

The mechanisms underlying myocardial ischaemia and reperfusion-induced injury have been investigated, mainly by using animal experimental preparations in vitro and in vivo, but little is known of the process in human myocardium. The present studies characterize an in vitro model using human myocardium for the study of early and delayed effects of ischaemia and reperfusion. The right atrial appendage was manually sliced and incubated in buffer through which was bubbled O2/CO2 (19:1, v/v) for various time periods. Lactate dehydrogenase (LDH) leakage, 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl-2H-tetrazolium bromide (MTT) reduction, oxygen consumption, nucleotide levels and tissue morphology were all investigated as markers of myocardial injury. The specimens remained stable and viable up to 24 h, but had significantly deteriorated by 48 h. The preparation responded to ischaemia in a time-related manner. Tissue viability was reduced by 25% after 30 min ischaemia, declined to 60% after 60 min ischaemia and to 75% after 120 min ischaemia. Interestingly, the tissue was more susceptible when ischaemia was induced after 24 h of aerobic incubation. The effects of the duration of reperfusion were investigated after a fixed 60 min ischaemic insult. The results of LDH leakage suggest that reperfusion injury is mainly sustained within the first 2 h of reperfusion. However, the results of MTT reduction show that there is a progressive decrease in tissue viability over the 24 h reperfusion period, possibly reflecting the occurrence of tissue necrosis and apoptosis at different reperfusion times. In conclusion, the data provide evidence that the incubation of human atrial tissue in vitro is stable, and slices are viable for at least 24 h, which permits the study of early and delayed consequences of ischaemia and reperfusion in the human myocardium.

Стилі APA, Harvard, Vancouver, ISO та ін.

18

Gao, Sumin, Leyun Zhan, Zhengchao Yang, Ruili Shi, Haobo Li, Zhengyuan Xia, Shiying Yuan, Qing-ping Wu, Tingting Wang, and Shanglong Yao. "Remote Limb Ischaemic Postconditioning Protects Against Myocardial Ischaemia/Reperfusion Injury in Mice: Activation of JAK/STAT3-Mediated Nrf2-Antioxidant Signalling." Cellular Physiology and Biochemistry 43, no. 3 (2017): 1140–51. http://dx.doi.org/10.1159/000481755.

Повний текст джерела

Анотація:

Background: This study aimed to evaluate the protective effect and mechanisms of remote limb ischaemic postconditioning (RIPostC) against myocardial ischaemia/reperfusion (IR) injury. Methods: Male mice underwent 45 min of coronary artery occlusion followed by 2 h of reperfusion. RIPostC was achieved by three cycles of 5 min of ischaemia and 5 min of reperfusion in the left hind limb at the start of the reperfusion period. After 2 h of cardiac reperfusion, myocardial infarct size, cardiac enzyme release, apoptosis and oxidative stress were assessed. Protein expression and phosphorylation were measured by Western blotting. Results: RIPostC significantly decreased cardiac IR injury, as reflected by reduced infarct size and cellular apoptosis (22.9 ± 3.3% vs 40.9 ± 6.2% and 13.4% ± 3.1% vs 26.2% ± 3.1%, respectively, both P < 0.01) as well as plasma creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) release (21.97 ± 4.08 vs 35.86 ± 2.91 ng/ml and 6.17 ± 0.58 vs 8.37 ± 0.89 U/ml, respectively, both P < 0.01) compared with the IR group. RIPostC significantly increased the phosphorylation of myocardial STAT3, Akt and eNOS (P < 0.01). In addition, RIPostC elevated the nuclear translocation of Nrf2 and the expression of HO-1 and reduced myocardial oxidative stress (P < 0.05). Interestingly, pretreatment with the JAK/STAT3 inhibitor AG490 blocked the cardioprotective effect of RIPostC accompanied by decreased phosphorylation of myocardial STAT3, Akt and eNOS (P < 0.05), decreased nuclear translocation of Nrf2 and expression of HO-1, as well as increased oxidative stress (P < 0.05). Conclusion: RIPostC attenuates apoptosis and protects against myocardial IR injury, possibly through the activation of JAK/STAT3-mediated Nrf2-antioxidant signalling.

Стилі APA, Harvard, Vancouver, ISO та ін.

19

Yuqin, Wang, and Wang Yuqin. "TETRANDRINE CONTROL PRO-INFLAMMATORY FACTOR TO REDUCE RAT MYOCARDIAL ISCHAEMIC/REPERFUSION INJURY." Heart 98, Suppl 2 (October 2012): E124.1—E124. http://dx.doi.org/10.1136/heartjnl-2012-302920b.35.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

20

Hill, Bradford G., Sunday O. Awe, Elena Vladykovskaya, Yonis Ahmed, Si-Qi Liu, Aruni Bhatnagar, and Sanjay Srivastava. "Myocardial ischaemia inhibits mitochondrial metabolism of 4-hydroxy-trans-2-nonenal." Biochemical Journal 417, no. 2 (December 23, 2008): 513–24. http://dx.doi.org/10.1042/bj20081615.

Повний текст джерела

Анотація:

Myocardial ischaemia is associated with the generation of lipid peroxidation products such as HNE (4-hydroxy-trans-2-nonenal); however, the processes that predispose the ischaemic heart to toxicity by HNE and related species are not well understood. In the present study, we examined HNE metabolism in isolated aerobic and ischaemic rat hearts. In aerobic hearts, the reagent [3H]HNE was glutathiolated, oxidized to [3H]4-hydroxynonenoic acid, and reduced to [3H]1,4-dihydroxynonene. In ischaemic hearts, [3H]4-hydroxynonenoic acid formation was inhibited and higher levels of [3H]1,4-dihydroxynonene and [3H]GS-HNE (glutathione conjugate of HNE) were generated. Metabolism of [3H]HNE to [3H]4-hydroxynonenoic acid was restored upon reperfusion. Reperfused hearts were more efficient at metabolizing HNE than non-ischaemic hearts. Ischaemia increased the myocardial levels of endogenous HNE and 1,4-dihydroxynonene, but not 4-hydroxynonenoic acid. Isolated cardiac mitochondria metabolized [3H]HNE primarily to [3H]4-hydroxynonenoic acid and minimally to [3H]1,4-dihydroxynonene and [3H]GS-HNE. Moreover, [3H]4-hydroxynonenoic acid was extruded from mitochondria, whereas other [3H]HNE metabolites were retained in the matrix. Mitochondria isolated from ischaemic hearts were found to contain 2-fold higher levels of protein-bound HNE than the cytosol, as well as increased [3H]GS-HNE and [3H]1,4-dihydroxynonene, but not [3H]4-hydroxynonenoic acid. Mitochondrial HNE oxidation was inhibited at an NAD+/NADH ratio of 0.4 (equivalent to the ischaemic heart) and restored at an NAD+/NADH ratio of 8.6 (equivalent to the reperfused heart). These results suggest that HNE metabolism is inhibited during myocardial ischaemia owing to NAD+ depletion. This decrease in mitochondrial metabolism of lipid peroxidation products and the inability of the mitochondria to extrude HNE metabolites could contribute to myocardial ischaemia/reperfusion injury.

Стилі APA, Harvard, Vancouver, ISO та ін.

21

Candilio, Luciano, and Derek Hausenloy. "Is there a role for ischaemic conditioning in cardiac surgery?" F1000Research 6 (April 25, 2017): 563. http://dx.doi.org/10.12688/f1000research.10963.1.

Повний текст джерела

Анотація:

Coronary artery disease (CAD) is a major cause of morbidity and mortality worldwide. Coronary artery bypass graft (CABG) surgery is the revascularisation strategy of choice in patients with diabetes mellitus and complex CAD. Owing to a number of factors, including the ageing population, the increased complexity of CAD being treated, concomitant valve and aortic surgery, and multiple comorbidities, higher-risk patients are being operated on, the result of which is an increased risk of sustaining perioperative myocardial injury (PMI) and poorer clinical outcomes. As such, new treatment strategies are required to protect the heart against PMI and improve clinical outcomes following cardiac surgery. In this regard, the heart can be endogenously protected from PMI by subjecting the myocardium to one or more brief cycles of ischaemia and reperfusion, a strategy called “ischaemic conditioning”. However, this requires an intervention applied directly to the heart, which may be challenging to apply in the clinical setting. In this regard, the strategy of remote ischaemic conditioning (RIC) may be more attractive, as it allows the endogenous cardioprotective strategy to be applied away from the heart to the arm or leg by simply inflating and deflating a cuff on the upper arm or thigh to induce one or more brief cycles of ischaemia and reperfusion (termed “limb RIC”). Although a number of small clinical studies have demonstrated less PMI with limb RIC following cardiac surgery, three recently published large multicentre randomised clinical trials found no beneficial effects on short-term or long-term clinical outcomes, questioning the role of limb RIC in the setting of cardiac surgery. In this article, we review ischaemic conditioning as a therapeutic strategy for endogenous cardioprotection in patients undergoing cardiac surgery and discuss the potential reasons for the failure of limb RIC to improve clinical outcomes in this setting. Crucially, limb RIC still has the therapeutic potential to protect the heart in other clinical settings, such as acute myocardial infarction, and it may also protect other organs against acute ischaemia/reperfusion injury (such as the brain, kidney, and liver).

Стилі APA, Harvard, Vancouver, ISO та ін.

22

Nakamura, Yuki, Shunsuke Saito, Shigeru Miyagawa, Yasushi Yoshikawa, Hiroki Hata, Daisuke Yoshioka, Koichi Toda, and Yoshiki Sawa. "Perioperative ischaemic reperfusion injury and allograft function in the early post-transplantation period." Interactive CardioVascular and Thoracic Surgery 29, no. 2 (March 28, 2019): 230–36. http://dx.doi.org/10.1093/icvts/ivz086.

Повний текст джерела

Анотація:

Abstract OBJECTIVES Ischaemic reperfusion injury (IRI) is an inevitable complication of heart transplantation (HTX) and is observed as a pathological finding in biopsies from transplanted allografts. The aim of this study was to evaluate the severity of IRI and determine the clinical outcomes of HTX in patients with severe IRI. METHODS We enrolled 74 consecutive patients who had undergone HTX since 2007. Endomyocardial biopsy samples were obtained from the right ventricle of the transplanted heart. IRI was graded as ‘trivial’, ‘mild’, ‘moderate’ or ‘severe’ according to the extent of IRI-specific findings in the samples. The cohort was divided into a moderate-to-severe IRI group with 21 patients [IRI(+)] and a low-grade group with 53 patients [IRI(−)]. RESULTS The frequency of mechanical circulatory support and duration of catecholamine dependence in the early postoperative period were significantly higher in the IRI(+) group compared to the IRI(−) group. However, overall survival after HTX and mid-term cardiac allograft function were not significantly different between the groups. Among perioperative factors, cardiac ischaemic time was significantly different between the groups [IRI(−) vs IRI(+), 199 ± 38 min vs 239 ± 39 min; P < 0.001]. Incremental increases in cardiac ischaemic time were correlated with increases in IRI severity. Serum troponin T levels 3 h after donor heart reperfusion was significantly correlated with cardiac ischaemic time (r = 0.418, P = 0.0007). CONCLUSIONS IRI is associated with a complicated clinical course in the early post-HTX period due to temporary deterioration of allograft function. This may be attributable to myocardial stunning caused by long donor heart ischaemic time during HTX.

Стилі APA, Harvard, Vancouver, ISO та ін.

23

Liu, Zhen-bing, Lin-feng Zhao, Dandan Hong, and Jun-ling Gao. "Remote ischaemic preconditioning reduces myocardial ischaemic reperfusion injury in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention." Acta Cardiologica 71, no. 5 (October 2016): 596–603. http://dx.doi.org/10.1080/ac.71.5.3167504.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

24

Cao, Fang, Sevasti Zervou, and Craig A. Lygate. "The creatine kinase system as a therapeutic target for myocardial ischaemia–reperfusion injury." Biochemical Society Transactions 46, no. 5 (September 21, 2018): 1119–27. http://dx.doi.org/10.1042/bst20170504.

Повний текст джерела

Анотація:

Restoring blood flow following an acute myocardial infarction saves lives, but results in tissue damage due to ischaemia–reperfusion injury (I/R). Ameliorating this damage is a major research goal to improve recovery and reduce subsequent morbidity due to heart failure. Both the ischaemic and reperfusion phases represent crises of cellular energy provision in which the mitochondria play a central role. This mini-review will explore the rationale and therapeutic potential of augmenting the creatine kinase (CK) energy shuttle, which constitutes the primary short-term energy buffer and transport system in the cardiomyocyte. Proof-of-principle data from several transgenic mouse models have demonstrated robust cardioprotection by either raising myocardial creatine levels or by overexpressing specific CK isoforms. The effect on cardiac function, high-energy phosphates and myocardial injury will be discussed and possible directions for future research highlighted. We conclude that the CK system represents a viable target for therapeutic intervention in I/R injury; however, much needed translational studies will require the development of new pharmacological tools.

Стилі APA, Harvard, Vancouver, ISO та ін.

25

Rossello, Xavier, Manuel Lobo-Gonzalez, and Borja Ibanez. "Editor’s Choice- Pathophysiology and therapy of myocardial ischaemia/reperfusion syndrome." European Heart Journal: Acute Cardiovascular Care 8, no. 5 (June 7, 2019): 443–56. http://dx.doi.org/10.1177/2048872619845283.

Повний текст джерела

Анотація:

There is a need to find interventions able to reduce the extent of injury in reperfused ST-segment elevation myocardial infarction (STEMI) beyond timely reperfusion. In this review, we summarise the clinical impact of STEMI from epidemiological, clinical and biological perspectives. We also revise the pathophysiology underlying the ischaemia/reperfusion syndrome occurring in reperfused STEMI, including the several players involved in this syndrome, such as cardiomyocytes, microcirculation and circulating cells. Interventions aimed to reduce the resultant infarct size, known as cardioprotective therapies, are extensively discussed, putting the focus on both mechanical interventions (i.e. ischaemic conditioning) and promising pharmacological therapies, such as early intravenous metoprolol, exenatide and other glucose modulators, N-acetylcysteine as well as on some other classic therapies which have failed to be translated to the clinical arena. Novel targets for evolving therapeutic interventions to ameliorate ischaemia/reperfusion injury are also discussed. Finally, we highlight the necessity to improve the study design of future randomised clinical trials in the field, as well as to select patients better who can most likely benefit from cardioprotective interventions.

Стилі APA, Harvard, Vancouver, ISO та ін.

26

Penna, Claudia, Saveria Femminò, Giuseppe Alloatti, Maria F. Brizzi, Tommaso Angelone, and Pasquale Pagliaro. "Extracellular Vesicles in Comorbidities Associated with Ischaemic Heart Disease: Focus on Sex, an Overlooked Factor." Journal of Clinical Medicine 10, no. 2 (January 17, 2021): 327. http://dx.doi.org/10.3390/jcm10020327.

Повний текст джерела

Анотація:

Extracellular vesicles (EV) are emerging early markers of myocardial damage and key mediators of cardioprotection. Therefore, EV are becoming fascinating tools to prevent cardiovascular disease and feasible weapons to limit ischaemia/reperfusion injury. It is well known that metabolic syndrome negatively affects vascular and endothelial function, thus creating predisposition to ischemic diseases. Additionally, sex is known to significantly impact myocardial injury and cardioprotection. Therefore, actions able to reduce risk factors related to comorbidities in ischaemic diseases are required to prevent maladaptive ventricular remodelling, preserve cardiac function, and prevent the onset of heart failure. This implies that early diagnosis and personalised medicine, also related to sex differences, are mandatory for primary or secondary prevention. Here, we report the contribution of EV as biomarkers and/or therapeutic tools in comorbidities predisposing to cardiac ischaemic disease. Whenever possible, attention is dedicated to data linking EV to sex differences.

Стилі APA, Harvard, Vancouver, ISO та ін.

27

Sharma, Shweta, Avileen Kaur, and Saurabh Sharma. "Preconditioning potential of purmorphamine: a hedgehog activator against ischaemic reperfusion injury in ovariectomised rat heart." Perfusion 33, no. 3 (October 24, 2017): 209–18. http://dx.doi.org/10.1177/0267659117732401.

Повний текст джерела

Анотація:

Objective: The present study was been designed to investigate the role and pharmacological potential of hedgehog in oestrogen-deficient rat heart. Methods: Oestrogen deficiency was produced in female Wistar rats by the surgical removal of both ovaries and these animals were used four weeks later. Isolated rat heart was subjected to 30 min ischaemia followed by 120 min of reperfusion (I/R). The heart was subjected to pharmacological preconditioning with the hedgehog agonist purmorphamine (1μM) and GDC-0449, a hedgehog antagonist, in the last episode of reperfusion before I/R. Myocardial infarction was assessed in terms of the increase in lactate dehydrogenase (LDH), creatinine kinase-MB (CK-MB), myeloperoxidase (MPO) level and infarct size (triphenyltetrazolium chloride staining). Immunohistochemistry analysis was done for the assessment of tumour necrosis factor (TNF)-α level in cardiac tissue. eNOS expression was estimated by rt-PCR. Results: Pharmacological preconditioning with purmorphamine significantly attenuated I/R-induced myocardial infarction, TNF-α, MPO level and release of LDH and CK-MB compared to the I/R control group. However, GDC-0449 prevented the ameliorative preconditioning effect of estradiol. Conclusion: It may be concluded that the hedgehog agonist purmorphamine prevents the ovariectomised heart from ischaemic reperfusion injury.

Стилі APA, Harvard, Vancouver, ISO та ін.

28

Wang, Y., and Y. Wang. "e0130 Tetrandrine control pro-inflammatory factor to reduce rat myocardial ischaemic/reperfusion injury." Heart 96, Suppl 3 (October 1, 2010): A42. http://dx.doi.org/10.1136/hrt.2010.208967.130.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

29

Heinen, André, Vera Welke, Friederike Behmenburg, Martin Stroethoff, Volker Stoldt, Till Hoffmann, Markus W. Hollmann, and Ragnar Huhn. "Haemotherapy with Fibrinogen for Perioperative Bleeding Prevention—A view on Arterial Thrombogenesis and Myocardial Infarction in the Rat In Vivo." Journal of Clinical Medicine 8, no. 6 (June 19, 2019): 880. http://dx.doi.org/10.3390/jcm8060880.

Повний текст джерела

Анотація:

Major blood loss during cardiac surgery is associated with increased morbidity and mortality. Clinical pilot studies indicated that preoperative fibrinogen supplementation reduces postoperative blood loss without increasing thrombotic complications. However, an increase in fibrinogen concentration might rather aggravate pre-existing thrombosis than increase the incidence of thrombotic events. Therefore, we investigated, in the present study, whether fibrinogen supplementation influences (1) arterial thrombus formation, (2) the extent of myocardial infarction and (3) the cardioprotective effect of ischaemic preconditioning. Arterial thrombogenesis of the femoral artery was induced by topic FeCl3 treatment in anaesthetised Wistar rats after pretreatment with 60 mg/kg (Fiblow), 120 mg/kg (Fibhigh) or vehicle (Con). Vessel blood flow was monitored, and time to vessel occlusion was analysed as a marker for arterial thrombogenesis. In addition, regional myocardial I/R injury was induced by temporary left coronary artery occlusion in rats pretreated with or without fibrinogen supplementation. In additional groups, ischaemic preconditioning (IPC) was induced by 3 cycles of 5 min of ischaemia/reperfusion. In all groups, myocardial infarct size was determined by triphenyltetrazoliumchlorid staining. Arterial thrombogenesis was not affected by fibrinogen pretreatment. No differences in time until vessel occlusion between Con, Fiblow and Fibhigh groups were observed. In addition, fibrinogen supplementation in low and high concentrations had no effect on infarct size after regional myocardial ischaemia and reperfusion (Fiblow: 66 ± 10%, Fibhigh: 62 ± 9%; each ns vs. Con). IPC reduced infarct size from 62 ± 14% to 34 ± 12% (p < 0.05 vs. Con). Furthermore, both fibrinogen concentrations did not affect cardioprotection by ischaemic preconditioning (Fiblow + IPC: 34 ± 11%, Fibhigh + IPC: 31 ± 13%; each ns vs. IPC). Haemotherapy with fibrinogen did not affect arterial thrombogenesis, myocardial infarction and the cardioprotective effect of ischaemic preconditioning.

Стилі APA, Harvard, Vancouver, ISO та ін.

30

Edwards, Helen V., John D. Scott, and George S. Baillie. "PKA phosphorylation of the small heat-shock protein Hsp20 enhances its cardioprotective effects." Biochemical Society Transactions 40, no. 1 (January 19, 2012): 210–14. http://dx.doi.org/10.1042/bst20110673.

Повний текст джерела

Анотація:

The small heat-shock protein Hsp20 (heat-shock protein 20), also known as HspB6, has been shown to protect against a number of pathophysiological cardiac processes, including hypertrophy and apoptosis. Following β-adrenergic stimulation and local increases in cAMP, Hsp20 is phosphorylated on Ser16 by PKA (protein kinase A). This covalent modification is required for many of its cardioprotective effects. Both Hsp20 expression levels and its phosphorylation on Ser16 are increased in ischaemic myocardium. Transgenic mouse models with cardiac-specific overexpression of Hsp20 that are subject to ischaemia/reperfusion show smaller myocardial infarcts, and improved recovery of contractile performance during the reperfusion phase, compared with wild-type mice. This has been attributed to Hsp20's ability to protect against cardiomyocyte necrosis and apoptosis. Phosphomimics of Hsp20 (S16D mutants) confer improved protection from β-agonist-induced apoptosis in the heart, whereas phospho-null mutants (S16A) provide no protection. Naturally occurring mutants of Hsp20 at position 20 (P20L substitution) are associated with markedly reduced Hsp20 phosphorylation at Ser16, and this lack of phosphorylation correlates with abrogation of Hsp20's cardioprotective effects. Therefore phosphorylation of Hsp20 at Ser16 by PKA is vital for the cardioprotective actions of this small heat-shock protein. Selective targeting of signalling elements that can enhance this modification represents an exciting new therapeutic avenue for the prevention and treatment of myocardial remodelling and ischaemic injury.

Стилі APA, Harvard, Vancouver, ISO та ін.

31

Zhou, Bin, Shaoqing Lei, Rui Xue, Yan Leng, Zhengyuan Xia, and Zhong-Yuan Xia. "DJ-1 overexpression restores ischaemic post-conditioning-mediated cardioprotection in diabetic rats: role of autophagy." Clinical Science 131, no. 11 (May 22, 2017): 1161–78. http://dx.doi.org/10.1042/cs20170052.

Повний текст джерела

Анотація:

IPO (ischaemic post-conditioning) is a promising method of alleviating myocardial IR (ischaemia-reperfusion) injury; however, IPO-mediated cardioprotection is lost in diabetic hearts via mechanisms that remain largely unclear. We hypothesized that decreased cardiac expression of DJ-1, a positive modulator of autophagy, compromises the effectiveness of IPO-induced cardioprotection in diabetic rats. Diabetic rats subjected to myocardial IR (30 min of coronary artery occlusion followed by 120 min of reperfusion) exhibited more severe myocardial injury, less cardiac autophagy, lower DJ-1 expression and AMPK (adenosine monophosphate-activated protein kinase)/mTOR (mammalian target of rapamycin) pathway activity than non-diabetic rats. IPO significantly attenuated myocardial injury and up-regulated cardiac DJ-1 expression, AMPK/mTOR activity and autophagy in non-diabetic rats but not in diabetic rats. AAV9 (adeno-associated virus 9)-mediated cardiac DJ-1 overexpression as well as pretreatment with the autophagy inducer rapamycin restored IPO-induced cardioprotection in diabetic rats, an effect accompanied by AMPK/mTOR activation and autophagy up-regulation. Combining HPO (hypoxic post-conditioning) with DJ-1 overexpression markedly attenuated HR (hypoxia-reoxygenation) injury in H9c2 cells with high glucose (HG, 30 mM) exposure, accompanied by AMPK/mTOR signalling activation and autophagy up-regulation. The DJ-1 overexpression-mediated preservation of HPO-induced cardioprotection was completely inhibited by the AMPK inhibitor compound C (CC) and the autophagy inhibitor 3-MA (3-methyladenine). Thus, decreased cardiac DJ-1 expression, which results in impaired AMPK/mTOR signalling and decreased autophagy, could be a major mechanism underlying the loss of IPO-induced cardioprotection in diabetes.

Стилі APA, Harvard, Vancouver, ISO та ін.

32

ZHANG, Jin-Gang, and Manuel GALIÑANES. "Role of the l-arginine/nitric oxide pathway in ischaemic/reoxygenation injury of the human myocardium." Clinical Science 99, no. 6 (November 7, 2000): 497–504. http://dx.doi.org/10.1042/cs0990497.

Повний текст джерела

Анотація:

The role of the L-arginine/nitric oxide (NO) pathway in myocardial ischaemic/reperfusion injury remains controversial in experimental animal models. The aim of the present studies was to investigate the role of this pathway in the human myocardium. Myocardial specimens from right atrial appendages of patients undergoing elective coronary bypass graft surgery were incubated in crystalloid buffer at 37 °C and subjected to 120 min of simulated ischaemia followed by 120 min of reoxygenation. Tested drugs were added 15 min before ischaemia, and maintained during ischaemia and throughout reoxygenation. Ischaemia resulted in severe myocardial damage, as assessed by the leakage of lactate dehydrogenase (LDH) into the incubation medium and by the capacity of the tissue to reduce 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) to formazan product. L-Arginine (10 mM), a precursor of NO, significantly decreased LDH leakage (from 9.0±0.6 to 5.3±0.3 units/g wet wt; P < 0.05), but had no effect on MTT reduction or oxygen consumption. D-Arginine (10 mM), NG-nitro-L-arginine methyl ester (L-NAME; 0.5 mM), an NO synthase inhibitor, and S-nitroso-N-acetylpenicillamine (at 1, 100, 500 and 1000 µM), an NO donor, had no significant effects on the measured indices, and L-NAME did not reverse the protection afforded by L-arginine against LDH leakage. In addition, the formation of nitrotyrosine was not influenced by ischaemia/reoxygenation alone or by the agents investigated. In conclusion, these data suggest that L-arginine affords modest protection against ischaemic/reoxygenation injury of the human myocardium, an action that is NO-independent, and that NO metabolism does not play a significant role in this model.

Стилі APA, Harvard, Vancouver, ISO та ін.

33

Zhao, X., and X. Yu. "Role of ischaemic postconditioning regulates endoplasmic reticulum stress in prevention of myocardial reperfusion injury." Heart 97, Suppl 3 (October 1, 2011): A127—A128. http://dx.doi.org/10.1136/heartjnl-2011-300867.370.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

34

Kupatt, Christian, Reinhard Wichels, BF Becker, and Peter Boekstegers. "Inhibition of post-ischaemic inflammation as a therapeutic approach to myocardial ischaemia reperfusion injury." Expert Opinion on Therapeutic Patents 10, no. 9 (September 2000): 1395–404. http://dx.doi.org/10.1517/13543776.10.9.1395.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

35

van Jaarsveld, H., J. M. Kuyl, and D. W. Alberts. "Antioxidant Vitamin Supplementation of Smoke-Exposed Rats Partially Protects Against Myocardial Ischaemic/Reperfusion Injury." Free Radical Research Communications 17, no. 4 (January 1992): 263–69. http://dx.doi.org/10.3109/10715769209079518.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

36

Dolman, John, and David V. Godin. "Myocardial ischaemic/ reperfusion injury in the anaesthetized rabbit: comparative effects of halothane and isoflurane." Canadian Anaesthetists’ Society Journal 33, no. 4 (July 1986): 443–52. http://dx.doi.org/10.1007/bf03010969.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

37

Doulamis, Ilias P., Alvise Guariento, Thomas Duignan, Arzoo Orfany, Takashi Kido, David Zurakowski, Pedro J. del Nido, and James D. McCully. "Mitochondrial transplantation for myocardial protection in diabetic hearts." European Journal of Cardio-Thoracic Surgery 57, no. 5 (November 28, 2019): 836–45. http://dx.doi.org/10.1093/ejcts/ezz326.

Повний текст джерела

Анотація:

Abstract OBJECTIVES Type 2 diabetes causes mitochondrial dysfunction, which increases myocardial susceptibility to ischaemia–reperfusion injury. We investigated the efficacy of transplantation of mitochondria isolated from diabetic or non-diabetic donors in providing cardioprotection from warm global ischaemia and reperfusion in the diabetic rat heart. METHODS Ex vivo perfused hearts from Zucker diabetic fatty (ZDF fa/fa) rats (n = 6 per group) were subjected to 30 min of warm global ischaemia and 120 min reperfusion. Immediately prior to reperfusion, vehicle alone (VEH) or vehicle containing mitochondria isolated from either ZDF (MTZDF) or non-diabetic Zucker lean (ZL +/?) (MTZL) skeletal muscle were delivered to the coronary arteries via the aortic cannula. RESULTS Following 30-min global ischaemia and 120-min reperfusion, left ventricular developed pressure was significantly increased in MTZDF and MTZL groups compared to VEH group (MTZDF: 92.8 ± 5.2 mmHg vs MTZL: 110.7 ± 2.4 mmHg vs VEH: 44.3 ± 5.9 mmHg; P < 0.01 each); and left ventricular end-diastolic pressure was significantly decreased (MTZDF 12.1 ± 1.3 mmHg vs MTZL 8.6 ± 0.8 mmHg vs VEH: 18.6 ± 1.5 mmHg; P = 0.016 for MTZDF vs VEH and P < 0.01 for MTZL vs VEH). Total tissue ATP content was significantly increased in both MT groups compared to VEH group (MTZDF: 18.9 ± 1.5 mmol/mg protein/mg tissue vs MTZL: 28.1 ± 2.3 mmol/mg protein/mg tissue vs VEH: 13.1 ± 0.5 mmol/mg protein/mg tissue; P = 0.018 for MTZDF vs VEH and P < 0.01 for MTZL vs VEH). Infarct size was significantly decreased in the MT groups (MTZDF: 11.8 ± 0.7% vs MTZL: 9.9 ± 0.5% vs VEH: 52.0 ± 1.4%; P < 0.01 each). CONCLUSIONS Mitochondrial transplantation significantly enhances post-ischaemic myocardial functional recovery and significantly decreases myocellular injury in the diabetic heart.

Стилі APA, Harvard, Vancouver, ISO та ін.

38

Huang, Kun, Ju Liu, Hui Zhang, Jiliang Wang, and Huili Li. "Intramyocardial Injection of siRNAs Can Efficiently Establish Myocardial Tissue-Specific Renalase Knockdown Mouse Model." BioMed Research International 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/1267570.

Повний текст джерела

Анотація:

Ischaemia/reperfusion (I/R) injury will cause additional death of cardiomyocytes in ischaemic heart disease. Recent studies revealed that renalase was involved in the I/R injury. So, the myocardial tissue-specific knockdown mouse models were needed for the investigations of renalase. To establish the mouse models, intramyocardial injection of siRNAs targeting renalase was performed in mice. The wild distribution and high transfection efficiency of the siRNAs were approved. And the renalase expression was efficiently suppressed in myocardial tissue. Compared with the high cost, time consumption, and genetic compensation risk of the Cre/loxP technology, RNA interference (RNAi) technology is much cheaper and less time-consuming. Among the RNAi technologies, injection of siRNAs is safer than virus. And considering the properties of the I/R injury mouse models, the efficiency and durability of injection with siRNAs are acceptable for the studies. Altogether, intramyocardial injection of siRNAs targeting renalase is an economical, safe, and efficient method to establish myocardial tissue-specific renalase knockdown mouse models.

Стилі APA, Harvard, Vancouver, ISO та ін.

39

Solskov, Lasse, Bo Løfgren, Rasmus Pold, Steen B. Kristiansen, Torsten T. Nielsen, David H. Overstreet, Ole Schmitz, Hans Erik Bøtker, Sten Lund, and Gregers Wegener. "Evaluation of the relationship between hyperinsulinaemia and myocardial ischaemia/reperfusion injury in a rat model of depression." Clinical Science 118, no. 4 (November 9, 2009): 259–67. http://dx.doi.org/10.1042/cs20090108.

Повний текст джерела

Анотація:

Major depression is associated with medical co-morbidity, such as ischaemic heart disease and diabetes, but the underlying pathophysiological mechanisms remain unclear. The FSL (Flinders Sensitive Line) rat is a genetic animal model of depression exhibiting features similar to those of depressed individuals. The aim of the present study was to compare the myocardial responsiveness to I/R (ischaemia/reperfusion) injury and the effects of IPC (ischaemic preconditioning) in hearts from FSL rats using SD (Sprague–Dawley) rats as controls and to characterize differences in glucose metabolism and insulin sensitivity between FSL and SD rats. Hearts were perfused in a Langendorff model and were subjected or not to IPC before 40 min of global ischaemia, followed by 120 min of reperfusion. Myocardial infarct size was found to be significantly larger in the FSL rats than in the SD rats following I/R injury (62.4±4.2 compared with 46.9±2.9%; P<0.05). IPC reduced the infarct size (P<0.01) and improved haemodynamic function (P<0.01) in both FSL and SD rats. No significant difference was found in blood glucose levels between the two groups measured after 12 h of fasting, but fasting plasma insulin (70.1±8.9 compared with 40.9±4.7 pmol/l; P<0.05) and the HOMA (homoeostatic model assessment) index (P<0.01) were significantly higher in FSL rats compared with SD rats. In conclusion, FSL rats had larger infarct sizes following I/R injury and were found to be hyperinsulinaemic compared with SD rats, but appeared to have a maintained cardioprotective mechanism against I/R injury, as IPC reduced infarct size in these rats. This animal model may be useful in future studies when examining the mechanisms that contribute to the cardiovascular complications associated with depression.

Стилі APA, Harvard, Vancouver, ISO та ін.

40

Xin, Z., Y. Xuefan, and Q. Nanhu. "e0123 The effect of diabetes on protection of ischaemic postconditioning in myocardial ischaemia-reperfusion injury." Heart 96, Suppl 3 (October 1, 2010): A40. http://dx.doi.org/10.1136/hrt.2010.208967.123.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

41

Auchampach, J. A., and G. J. Gross. "Anti-ischaemic actions of potassium channel openers in experimental myocardial ischaemia/reperfusion injury in dogs." European Heart Journal 14, suppl B (July 2, 1993): 10–15. http://dx.doi.org/10.1093/eurheartj/14.suppl_b.10.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

42

Przyklenk, K., and RA Kloner. "Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury." British Journal of Clinical Pharmacology 28, S2 (1989): 167S—175S. http://dx.doi.org/10.1111/j.1365-2125.1989.tb03592.x.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

43

Pernow and Wang. "The role of the L -arginine/nitric oxide pathway in myocardial ischaemic and reperfusion injury." Acta Physiologica Scandinavica 167, no. 2 (October 1999): 151–59. http://dx.doi.org/10.1046/j.1365-201x.1999.00588.x.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

44

Thomas, C., B. Feehan, and C. May. "Remote limb ischaemic preconditioning: contribution of vagal innervation to protection against myocardial ischaemia-reperfusion injury." Heart, Lung and Circulation 24 (2015): S164. http://dx.doi.org/10.1016/j.hlc.2015.06.124.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

45

Tuter, Denis S., Philippe Y. Kopylov, Abram L. Syrkin, Oleg S. Glazachev, Roman N. Komarov, Andrei I. Katkov, Ljudmila P. Severova, Ekaterina V. Ivanova, Young Zhang, and Hugo Saner. "Intermittent systemic hypoxic–hyperoxic training for myocardial protection in patients undergoing coronary artery bypass surgery: first results from a single-centre, randomised controlled trial." Open Heart 5, no. 2 (November 2018): e000891. http://dx.doi.org/10.1136/openhrt-2018-000891.

Повний текст джерела

Анотація:

BackgroundAlthough remote ischaemic preconditioning (RIP) provides protection against myocardial ischaemia and reperfusion injury during cardiac surgery, it is not widely used. Systemic intermittent hypoxic–hyperoxic training (IHHT) may be a suitable alternative.MethodsThis is a prospective, single-centre, randomised controlled trial. 127 patients with ischaemic heart disease and indication for coronary artery bypass graft (CABG) surgery from the Cardiology Clinic IM Sechenov First Moscow State Medical University were randomly assigned to IHHT, IHHT-control or RIP. Primary endpoint was serum concentration of troponin I and lactate 2 and 24 hours after surgery.ResultsMedian value for troponin I 24 hours after surgery was 1.068 (0.388–1.397) ng/mL in the IHHT group and was significantly lower compared with IHHT-controls with 1.980 (1.068–3.239) ng/mL (p=0.012) and to the RIP group with 1.762 (1.288–2.186) ng/mL (p=0.029), while there was no significant difference between RIP and the IHHT-control. Serum lactate after surgery was 1.74 (1.23–2.04) mmol/L in the IHHT group and was also significantly lower compared with IHHT-controls with 2.10 (1.80–2.29) mmol/L (p=0.045) and RIP with 2.12 (1.91–2.33) mmol/L (p=0.032). No significant complications or serious adverse events were observed during IHHT. Intraoperative and early postoperative complications did not differ significantly between groups.ConclusionsThe results of this first trial using IHHT for myocardial protection against perioperative ischaemic myocardial injury in patients undergoing CABG surgery are promising and further larger trials should be done with adequate power to detect clinical rather than surrogate marker benefits.

Стилі APA, Harvard, Vancouver, ISO та ін.

46

Mukherjee, Subhendu, Istvan Lekli, Diptarka Ray, Hiranmoy Gangopadhyay, Utpal Raychaudhuri, and Dipak K. Das. "Comparison of the protective effects of steamed and cooked broccolis on ischaemia–reperfusion-induced cardiac injury." British Journal of Nutrition 103, no. 6 (October 27, 2009): 815–23. http://dx.doi.org/10.1017/s0007114509992492.

Повний текст джерела

Анотація:

Recently, broccoli, a vegetable of the Brassica family, has been found to protect the myocardium from ischaemic reperfusion injury through the redox signalling of sulphoraphane, which is being formed from glucosinolate present in this vegetable. Since cooked broccoli loses most of its glucosinolate, we assumed that fresh broccoli could be a superior cardioprotective agent compared to cooked broccoli. To test this, two groups of rats were fed with fresh (steamed) broccoli or cooked broccoli for 30 d, while a third group was given vehicle only for the same period of time. After 30 d, all the rats were sacrificed, and the isolated working hearts were subjected to 30 min ischaemia followed by 2 h of reperfusion. Both cooked and steamed broccolis displayed significantly improved post-ischaemic ventricular function and reduced myocardial infarction and cardiomyocyte apoptosis compared to control, but steamed broccoli showed superior cardioprotective abilities compared with the cooked broccoli. Corroborating with these results, both cooked and steamed broccolis demonstrated significantly enhanced induction of the survival signalling proteins including Bcl2, Akt, extracellular signal-regulated kinase 1/2, haemoxygenase-1, NFE2 related factor 2, superoxide dismutase (SOD1) and SOD2 and down-regulation of the proteins (e.g. Bax, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase) of the death signalling pathway, steamed broccoli displaying superior results over its cooked counterpart. The expressions of proteins of the thioredoxin (Trx) superfamily including Trx1 and its precursor sulphoraphane, Trx2 and Trx reductase, were enhanced only in the steamed broccoli group. The results of the present study documented superior cardioprotective properties of the steamed broccoli over cooked broccoli because of the ability of fresh broccoli to perform redox signalling of Trx.

Стилі APA, Harvard, Vancouver, ISO та ін.

47

Cabrera-Fuentes, Hector, Javier Inserte, Mona Saffarzadeh, Sebastian Galuska, Vijith Vijayan, Ignasi Barba, Guillermo Barreto та ін. "RNase1 prevents the damaging interplay between extracellular RNA and tumour necrosis factor-α in cardiac ischaemia/reperfusion injury". Thrombosis and Haemostasis 112, № 12 (2014): 1110–19. http://dx.doi.org/10.1160/th14-08-0703.

Повний текст джерела

Анотація:

SummaryDespite optimal therapy, the morbidity and mortality of patients presenting with an acute myocardial infarction (MI) remain significant, and the initial mechanistic trigger of myocardial “ischaemia/reperfusion (I/R) injury” remains greatly unexplained. Here we show that factors released from the damaged cardiac tissue itself, in particular extracellular RNA (eRNA) and tumour-necrosis-factor α (TNF-α), may dictate I/R injury. In an experimental in vivo mouse model of myocardial I/R as well as in the isolated I/R Langendorff-perfused rat heart, cardiomyocyte death was induced by eRNA and TNF-α. Moreover, TNF-α promoted further eRNA release especially under hypoxia, feeding a vicious cell damaging cycle during I/R with the massive production of oxygen radicals, mitochondrial obstruction, decrease in antioxidant enzymes and decline of cardiomyocyte functions. The administration of RNase1 significantly decreased myocardial infarction in both experimental models. This regimen allowed the reduction in cytokine release, normalisation of antioxidant enzymes as well as preservation of cardiac tissue. Thus, RNase1 administration provides a novel therapeutic regimen to interfere with the adverse eRNA-TNF-α interplay and significantly reduces or prevents the pathological outcome of ischaemic heart disease.

Стилі APA, Harvard, Vancouver, ISO та ін.

48

Jh, Erlich, Boyle Em, Santucci Ra, Kovacich Jc, Labriola J, Fearns C, Morgan En, et al. "INHIBITION OF TISSUE FACTOR EXPRESSED BY ISCHAEMIC CARDIOMYOCYTES REDUCES INFARCT SIZE AFTER MYOCARDIAL ISCHEMIA/REPERFUSION INJURY." Nephrology 5, no. 3 (October 2000): A105. http://dx.doi.org/10.1046/j.1440-1797.2000.005003a105.x.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

49

Ruiz-Meana, Marisol, Diana Bou-Teen, Péter Ferdinandy, Mariann Gyongyosi, Maurizio Pesce, Cinzia Perrino, Rainer Schulz, et al. "Cardiomyocyte ageing and cardioprotection: consensus document from the ESC working groups cell biology of the heart and myocardial function." Cardiovascular Research 116, no. 11 (May 8, 2020): 1835–49. http://dx.doi.org/10.1093/cvr/cvaa132.

Повний текст джерела

Анотація:

Abstract Advanced age is a major predisposing risk factor for the incidence of coronary syndromes and comorbid conditions which impact the heart response to cardioprotective interventions. Advanced age also significantly increases the risk of developing post-ischaemic adverse remodelling and heart failure after ischaemia/reperfusion (IR) injury. Some of the signalling pathways become defective or attenuated during ageing, whereas others with well-known detrimental consequences, such as glycoxidation or proinflammatory pathways, are exacerbated. The causative mechanisms responsible for all these changes are yet to be elucidated and are a matter of active research. Here, we review the current knowledge about the pathophysiology of cardiac ageing that eventually impacts on the increased susceptibility of cells to IR injury and can affect the efficiency of cardioprotective strategies.

Стилі APA, Harvard, Vancouver, ISO та ін.

50

Tucker, Bradley, Kaivan Vaidya, Blake J. Cochran, and Sanjay Patel. "Inflammation during Percutaneous Coronary Intervention—Prognostic Value, Mechanisms and Therapeutic Targets." Cells 10, no. 6 (June 4, 2021): 1391. http://dx.doi.org/10.3390/cells10061391.

Повний текст джерела

Анотація:

Periprocedural myocardial injury and myocardial infarction (MI) are not infrequent complications of percutaneous coronary intervention (PCI) and are associated with greater short- and long-term mortality. There is an abundance of preclinical and observational data demonstrating that high levels of pre-, intra- and post-procedural inflammation are associated with a higher incidence of periprocedural myonecrosis as well as future ischaemic events, heart failure hospitalisations and cardiac-related mortality. Beyond inflammation associated with the underlying coronary pathology, PCI itself elicits an acute inflammatory response. PCI-induced inflammation is driven by a combination of direct endothelial damage, liberation of intra-plaque proinflammatory debris and reperfusion injury. Therefore, anti-inflammatory medications, such as colchicine, may provide a novel means of improving PCI outcomes in both the short- and long-term. This review summarises periprocedural MI epidemiology and pathophysiology, evaluates the prognostic value of pre-, intra- and post-procedural inflammation, dissects the mechanisms involved in the acute inflammatory response to PCI and discusses the potential for periprocedural anti-inflammatory treatment.

Стилі APA, Harvard, Vancouver, ISO та ін.

Статті в журналах з теми "Myocardial ischaemic-reperfusion injury"

Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями