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Published: 4 June 2021
Last updated: 20 February 2023

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1

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.

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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.
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2

Fernandez-Sanz, Celia, José Castellano, Elisabet Miro-Casas, Estefanía Nuñez, Javier Inserte, Jesús Vázquez, David Garcia-Dorado, and Marisol Ruiz-Meana. "Altered FoF1 ATP synthase and susceptibility to mitochondrial permeability transition pore during ischaemia and reperfusion in aging cardiomyocytes." Thrombosis and Haemostasis 113, no. 03 (May 2015): 441–51. http://dx.doi.org/10.1160/th14-10-0901.

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SummaryAging is a major determinant of the incidence and severity of ischaemic heart disease. Preclinical information suggests the existence of intrinsic cellular alterations that contribute to ischaemic susceptibility in senescent myocardium, by mechanisms not well established. We investigated the role of altered mitochondrial function in the adverse effect of aging. Isolated perfused hearts from old mice (> 20 months) displayed increased ischaemia-reperfusion injury as compared to hearts from adult mice (6 months) despite delayed onset of ischaemic rigor contracture. In cardiomyocytes from aging hearts there was a more rapid decline of mitochondrial membrane potential (ΔΨm) as compared to young ones, but ischaemic rigor shortening was also delayed. Transient recovery of ΔΨm observed during ischaemia, secondary to the reversal of mitochondrial FoF1 ATP synthase to ATPase mode, was markedly reduced in aging cardiomyocytes. Proteomic analysis demonstrated increased oxidation of different subunits of ATP synthase. Altered bionergetics in aging cells was associated with reduced mitochondrial calcium uptake and more severe cytosolic calcium overload during ischaemia-reperfusion. Despite attenuated ROS burst and mitochondrial calcium overload, mitochondrial permeability transition pore (mPTP) opening and cell death was increased in reperfused aged cells. In vitro studies demonstrated a significantly reduced calcium retention capacity in interfibrillar mitochondria from aging hearts. Our results identify altered FoF1 ATP synthase and increased sensitivity of mitochondria to undergo mPTP opening as important determinants of the reduced tolerance to ischaemia-reperfusion in aging hearts. Because ATP synthase has been proposed to conform mPTP, it is tempting to hypothesise that oxidation of ATP synthase underlie both phenomena.
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3

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.

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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.
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4

GOODWIN, Andrew T., Mahboob A. KHAN, Adrian H. CHESTER, Mohamed AMRANI, and Magdi H. YACOUB. "Up-regulation of endothelin-converting-enzyme mRNA expression following cardioplegic arrest." Clinical Science 103, s2002 (September 1, 2002): 206S—209S. http://dx.doi.org/10.1042/cs103s206s.

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Endothelin-1 (ET-1) is believed to play an important role in cardiac ischaemia/reperfusion injury. ET-1 is synthesized from preproET-1 by the action of ET-converting enzyme (ECE). It is unclear to what extent the ET system is activated following prolonged ischaemia. In this study we used a model mimicking the conditions of the donor heart during transplantation. Isolated rat hearts perfused with Krebs–Henseleit buffer were subjected to 30min of normothermic perfusion, then 4h of cardioplegic arrest at 4°C with St Thomas' Hospital solution, followed by reperfusion for 2h. Hearts were freeze-clamped at different time points during the protocol. Using quantitative reverse transcription–PCR, relative levels of ET-1 and ECE mRNA expression were measured and compared with a housekeeping gene (ribosomal protein L32). During reperfusion there was a consistent decrease in coronary flow to approx. 85–90% of pre-ischaemic flow. There was no significant alteration in preproET-1 mRNA expression during 2h of reperfusion. However, ECE mRNA expression was increased by 77.5% at 1h and by 74.6% at 2h following ischaemia compared with pre-ischaemic values (P<0.05). Thus we conclude that ECE mRNA expression is increased following prolonged hypothermic cardioplegic arrest. Elevations in the expression of this enzyme may help to explain the role of the ET system in the pathogenesis of ischaemia/reperfusion injury following cardiac surgery and transplantation.
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5

Sumegi, B., N. B. Butwell, C. R. Malloy, and A. D. Sherry. "Lipoamide influences substrate selection in post-ischaemic perfused rat hearts." Biochemical Journal 297, no. 1 (January 1, 1994): 109–13. http://dx.doi.org/10.1042/bj2970109.

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We investigated whether lipoamide and diacetyl-lipoamide are able to change the substrate selection in post-ischaemic myocardium. This can be important, because shifting heart metabolism from fatty acid to carbohydrate oxidation can decrease ischaemic injury. Studying the metabolism of [1,2-13C]diacetyl-lipoamide in situ in perfused rat heart by 13C n.m.r., we found intense 13C labelling in glutamate and aspartate, showing that acetyl groups from diacetyl-lipoamide are effectively transferred to CoA and metabolized in heart tissue. From analysis of glutamate C-3 and C-4 isotopomers, we determined the [1,2-13C]acetate/[3-13C]lactate utilization ratio in normoxic and post-ischaemic hearts, where under our experimental conditions the acetate/lactate utilization ratios were 1.2 +/- 0.2 and 2.4 +/- 0.3 in normoxic and post-ischaemic hearts respectively. When 0.25 mM lipoamide was added to the perfusate the acetate/lactate utilization ratio decreased to 1.4 +/- 0.1, which is almost equal to that found for normoxic hearts, showing that lipoamide increased the lactate utilization. In accordance with these data, we found that lipoamide activated pyruvate dehydrogenase by 50% in post-ischaemic myocardium. Competition between [3-13C]lactate and unlabelled octanoate was also studied in post-ischaemic hearts, and we found that lipoamide increased lactate utilization by 100% and increased the rate of the tricarboxylic acid cycle by 64%. Under the same experimental conditions, lipoamide significantly promoted the recovery of post-ischaemic unpaced hearts, showing the positive effect of increased lactate oxidation in post-ischaemic myocardium.
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6

Brander, L., D. Weinberger, and C. Henzen. "Heart and Brain: A Case of Focal Myocytolysis in Severe Pneumococcal Meningoencephalitis with Review of the Contemporary Literature." Anaesthesia and Intensive Care 31, no. 2 (April 2003): 202–7. http://dx.doi.org/10.1177/0310057x0303100212.

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We report electrocardiographic changes mimicking myocardial ischaemia in a 73-year-old man with fatal pneumococcal meningoencephalitis, present the autopsy-confirmed histological picture of extensive focal myocytolysis (contraction band necrosis) without myocardial infarction or myocarditis, and review the contemporary literature. Potentially reversible, probably non-ischaemic myocardial dysfunction may occur in association with acute noncardiac illnesses, such as brain injuries. Biochemical and morphological abnormalities in acutely failing hearts from head-injured organ donors point to specific pathophysiological mechanisms, which are different from heart failure from other causes. Sepsis-related factors may add to the myocardial dysfunction in patients with brain injury from meningoencephalitis.
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7

Uthman, Laween, Rianne Nederlof, Otto Eerbeek, Antonius Baartscheer, Cees Schumacher, Ninée Buchholtz, Markus W. Hollmann, Ruben Coronel, Nina C. Weber, and Coert J. Zuurbier. "Delayed ischaemic contracture onset by empagliflozin associates with NHE1 inhibition and is dependent on insulin in isolated mouse hearts." Cardiovascular Research 115, no. 10 (January 12, 2019): 1533–45. http://dx.doi.org/10.1093/cvr/cvz004.

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Abstract Aims Sodium glucose cotransporter 2 (SGLT2) inhibitors have sodium–hydrogen exchanger (NHE) inhibition properties in isolated cardiomyocytes, but it is unknown whether these properties extend to the intact heart during ischaemia–reperfusion (IR) conditions. NHE inhibitors as Cariporide delay time to onset of contracture (TOC) during ischaemia and reduce IR injury. We hypothesized that, in the ex vivo heart, Empagliflozin (Empa) mimics Cariporide during IR by delaying TOC and reducing IR injury. To facilitate translation to in vivo conditions with insulin present, effects were examined in the absence and presence of insulin. Methods and results Isolated C57Bl/6NCrl mouse hearts were subjected to 25 min I and 120 min R without and with 50 mU/L insulin. Without insulin, Empa and Cari delayed TOC by 100 and 129 s, respectively, yet only Cariporide reduced IR injury [infarct size (mean ± SEM in %) from 51 ± 6 to 34 ± 5]. Empa did not delay TOC in the presence of the NHE1 inhibitor Eniporide. Insulin perfusion increased tissue glycogen content at baseline (from 2 ± 2 µmol to 42 ± 1 µmol glycosyl units/g heart dry weight), amplified G6P and lactate accumulation at end-ischaemia, thereby decreased mtHKII and exacerbated IR injury. Under these conditions, Empa (1 µM) and Cariporide (10 µM) were without effect on TOC and IR injury. Empa and Cariporide both inhibited NHE activity, in isolated cardiomyocytes, independent of insulin. Conclusions In the absence of insulin, Empa and Cariporide strongly delayed the time to onset of contracture during ischaemia. In the presence of insulin, both Empa and Cari were without effect on IR, possibly because of severe ischaemic acidification. Insulin exacerbates IR injury through increased glycogen depletion during ischaemia and consequently mtHKII dissociation. The data suggest that also in the ex vivo intact heart Empa exerts direct cardiac effects by inhibiting NHE during ischaemia, but not during reperfusion.
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8

van der Kraaij, A. M., J. F. Koster, and W. R. Hagen. "Reappraisal of the e.p.r. signals in (post)-ischaemic cardiac tissue." Biochemical Journal 264, no. 3 (December 15, 1989): 687–94. http://dx.doi.org/10.1042/bj2640687.

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The present study was designed to measure directly, using e.p.r. spectroscopy, oxygen-derived free radicals in (post)-ischaemic or (post)-anoxic rat hearts. Rat hearts were rapidly freeze-clamped at 77 K under normoxic, anoxic, ischaemic or reperfusion conditions. The samples were measured at three different temperatures (13, 77 and 115 K) and at several microwave power levels, and were compared with isolated rat heart mitochondria. Samples were prepared both by grinding and as tissue cuts. The two preparation techniques gave identical e.p.r. results, which excludes the occurrence of grinding artifacts. No free radical signals linked to reperfusion injury were detected. Several electron transfer centres known in the mitochondrial respiratory chain were measured. The signals previously assigned to post-ischaemic reperfusion injury were found to originate from electron transfer centres of the respiratory chain, predominantly the iron-sulphur cluster S-1 in succinate dehydrogenase. The differences in signal intensity between normoxic, ischaemic and reperfused hearts were found to result from the different redox stages of these centres under the various conditions tested. These findings do not necessarily imply that oxygen-derived free radicals are not formed in cardiac tissue during (post)-ischaemic reperfusion. The constitutive background of paramagnetism from the respiratory chain, however, seriously hampers the direct detection of comparatively low concentrations of free radicals in cardiac tissue. It is therefore expedient to focus future experiments in this field on the use of spin-trapping agents.
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9

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.

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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.
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10

Wang, Q. D., A. Swärdh, and P. O. Sjöquist. "Relationship between ischaemic time and ischaemia/reperfusion injury in isolated Langendorff-perfused mouse hearts." Acta Physiologica Scandinavica 171, no. 2 (February 19, 2001): 123–28. http://dx.doi.org/10.1046/j.1365-201x.2001.00788.x.

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11

Takahashi, S., A. C. Barry, and S. M. Factor. "Collagen degradation in ischaemic rat hearts." Biochemical Journal 265, no. 1 (January 1, 1990): 233–41. http://dx.doi.org/10.1042/bj2650233.

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Myocardial extracellular matrix is organized into a complex arrangement of intercellular and pericellular fibres and fibrils that serves as a supporting framework for contracting cells. Recent evidence suggests that changes in ventricular shape and function occurring after ischaemic injury may be related to alterations of this matrix. In this report we describe the rapid and extensive loss of collagen in myocardial infarction produced by ligating the left anterior descending coronary artery of the rat for 1-3 h. The total collagen content in the myocardial infarct zones after 1, 2 and 3 h of ligation was 75 +/- 8%, 65 +/- 7% and 50 +/- 10% respectively (mean +/- S.D.) of that of either the non-infarcted tissue controls or of the same regions in sex- and age-matched normal left ventricles. A marked decrease also occurred in the residual collagens which were not extractable with 6 M-guanidine hydrochloride, suggesting that rapid degradation of insoluble collagen fibres may also occur. The decreased collagen content in the 3 h myocardial infarct coincided with the appearance of several enzyme activities. Collagenase, other neutral proteinase and presumed lysosomal serine proteinase activities were increased by 3, 3 and 2 times the control values respectively. These results suggest that the increased activities of collagenase and other neutral proteinases may be responsible for the rapid degradation of extracellular matrix collagen in myocardial infarct.
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12

Ravingerová, Táňa, Slávka Čarnická, Martina Nemčeková, Veronika Ledvényiová, Adriana Adameová, Tara Kelly, Eleftheria Barlaka, Eleftheria Galatou, Vinoth Kumar Megraj Khandelwal, and Antigone Lazou. "PPAR-alpha activation as a preconditioning-like intervention in rats in vivo confers myocardial protection against acute ischaemia–reperfusion injury: involvement of PI3K–Akt." Canadian Journal of Physiology and Pharmacology 90, no. 8 (August 2012): 1135–44. http://dx.doi.org/10.1139/y2012-052.

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Peroxisome proliferator-activated receptors (PPAR) regulate the expression of genes involved in lipid metabolism, energy production, and inflammation. Their role in ischaemia–reperfusion (I/R) is less clear, although research indicates involvement of PPARs in some forms of preconditioning. This study aimed to explore the effects of PPAR-α activation on the I/R injury and potential cardioprotective downstream mechanisms involved. Langendorff-perfused hearts of rats pretreated with the selective PPAR-α agonist WY-14643 (WY, pirinixic acid; 3 mg·(kg body mass)·day–1; 5 days) were subjected to 30 min ischaemia – 2 h reperfusion with or without the phosphatidylinositol 3-kinase (PI3K)–Akt inhibitor wortmannin for the evaluation of functional (left ventricular developed pressure, LVDP) recovery, infarct size (IS), and reperfusion-induced arrhythmias. A 2-fold increase in baseline PPAR-α mRNA levels (qPCR) in the WY-treated group and higher post-I/R PPAR-α levels compared with those in untreated controls were accompanied by similar changes in the expression of PPAR-α target genes PDK4 and mCPT-1, regulating glucose and fatty acid metabolism, and by enhanced Akt phosphorylation. Post-ischaemic LVDP restoration in WY-treated hearts reached 60% ± 9% of the pre-ischaemic values compared with 24% ± 3% in the control hearts (P < 0.05), coupled with reduced IS and incidence of ventricular fibrillation that was blunted by wortmannin. Results indicate that PPAR-α up-regulation may confer preconditioning-like protection via metabolic effects. Downstream mechanisms of PPAR-α-mediated cardioprotection may involve PI3K–Akt activation.
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Matejíková, Jana, Táňa Ravingerová, Dezider Pancza, Slávka Čarnická, and František Kolář. "Mitochondrial KATP opening confers protection against lethal myocardial injury and ischaemia-induced arrhythmias in the rat heart via PI3K/Akt-dependent and -independent mechanismsThis article is one of a selection of papers published in a special issue on Advances in Cardiovascular Research." Canadian Journal of Physiology and Pharmacology 87, no. 12 (December 2009): 1055–62. http://dx.doi.org/10.1139/y09-100.

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Opening of mitochondrial KATP channels (mitoKATP) has been reported to underlie protection against ischaemia–reperfusion injury induced by ischaemic preconditioning (I-PC); however, the molecular mechanisms of its antiarrhythmic effect have not been fully elucidated. We explored the involvement of phosphatidylinositol 3-kinase (PI3K)/Akt in the PC-like effect of mitoKATP opener diazoxide with particular regard to its role in protection against ischaemia-induced arrhythmias. Langendorff-perfused rat hearts were subjected to 30 min LAD occlusion with or without a prior 15 min of perfusion with diazoxide (50 µmol/L) given either alone (D-PC) or in combination with the PI3K/Akt inhibitor wortmannin (100 nmol/L). In an additional protocol, ischaemia was followed by 2 h reperfusion for infarct size (IS) determination (tetrazolium staining). The total number of premature ventricular complexes over the whole period of ischaemia, episodes of ventricular tachycardia and its duration were significantly lower in the D-PC group than in the non-preconditioned controls (158 ± 20, 2 ± 0.6 and 4.6 ± 1.8 s vs. 551 ± 61, 11 ± 2 and 42 ± 8 s, respectively; p < 0.05), concomitant with a 62% reduction in the size of infarction. Wortmannin modified neither arrhythmogenesis nor IS in the non-preconditioned hearts. Bracketing of diazoxide with wortmannin did not reverse the antiarrhythmic protection, whereas the IS-limiting effect was blunted. The results indicate that in contrast with the positive role of PI3K/Akt in protection against lethal myocardial injury, its activity is not involved in suppression of ischaemia-induced arrhythmias conferred by mitoKATP opening in the rat heart.
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14

Ryan, Kevin J. P., Matthew J. Elmes, and Simon C. Langley-Evans. "The Effects of Prenatal Protein Restriction onβ-Adrenergic Signalling of the Adult Rat Heart during Ischaemia Reperfusion." Journal of Nutrition and Metabolism 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/397389.

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A maternal low-protein diet (MLP) fed during pregnancy leads to hypertension in adult rat offspring. Hypertension is a major risk factor for ischaemic heart disease. This study examined the capacity of hearts from MLP-exposed offspring to recover from myocardial ischaemia-reperfusion (IR) and related this to cardiac expression of β-adrenergic receptors (β-AR) and their associated G proteins. Pregnant rats were fed control (CON) or MLP diets (n=12each group) throughout pregnancy. When aged 6 months, hearts from offspring underwent Langendorff cannulation to assess contractile function during baseline perfusion, 30 min ischemia and 60 min reperfusion. CON male hearts demonstrated impaired recovery in left ventricular pressure (LVP) anddP/dtmax(P<0.01) during reperfusion when compared to MLP male hearts. Maternal diet had no effect on female hearts to recover from IR. MLP males exhibited greater membrane expression ofβ2-AR following reperfusion and urinary excretion of noradrenaline and dopamine was lower in MLP and CON female rats versus CON males. In conclusion, the improved cardiac recovery in MLP male offspring following IR was attributed to greater membrane expression ofβ2-AR and reduced noradrenaline and dopamine levels. In contrast, females exhibiting both decreased membrane expression ofβ2-AR and catecholamine levels were protected from IR injury.
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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.

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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 &lt; 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 &lt; 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 &lt; 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 &lt; 0.01 each). CONCLUSIONS Mitochondrial transplantation significantly enhances post-ischaemic myocardial functional recovery and significantly decreases myocellular injury in the diabetic heart.
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Elmes, Matthew J., Andrea Haase, David S. Gardner, and Simon C. Langley-Evans. "Sex differences in sensitivity to β-adrenergic agonist isoproterenol in the isolated adult rat heart following prenatal protein restriction." British Journal of Nutrition 101, no. 5 (July 1, 2008): 725–34. http://dx.doi.org/10.1017/s0007114508025075.

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Hypertension is a major risk factor for the development of CVD. Epidemiological studies have shown that low birth weight increases the risk of developing hypertension in adulthood. Hypertension increases the risk of suffering IHD and early findings provide evidence that hearts from prenatally protein-restricted, hypertensive, male offspring are more susceptible to cardiac dysfunction following ischaemic events. Hypertension and abnormalities in cardiac function following ischaemia–reperfusion in the human population are treated therapeutically with β-adrenergic antagonists. We hypothesised that increased susceptibility to myocardial ischaemia–reperfusion injury in prenatally programmed offspring may be due to sympathetic hyperactivity. Pregnant Wistar rats were fed control or low-protein (maternal low protein; MLP) diets throughout gestation. At age 6 months, hearts were rapidly excised and retro-perfused using the Langendorff apparatus, to assess isolated cardiac function following stimulation with increasing doses of the non-specific β-agonist isoproterenol. Baseline heart rates were similar in control and MLP-fed offspring. With significant diet × sex interactions (P < 0·01) maximum heart rate response following isoproterenol infusion was significantly longer in MLP than control. Prenatal diet had no effect on maximal left ventricular developed pressure (LVDP) response, but the LVDP isoproterenol response was significantly longer in duration in MLP-exposed male offspring (diet × sex P < 0·001). Myocardial mRNA expression of β2-adrenergic receptors was increased in 2-week-old female MLP offspring only (P < 0·049). In conclusion, maternal protein restriction programmes cardiac sympathetic activity in a sex-specific manner, and may explain increased susceptibility to ischaemia–reperfusion injury in males subject to fetal undernutrition.
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17

Ravingerová, Táňa, Adriana Adameová, Tara Kelly, Efthymia Antonopoulou, Dezider Pancza, Mária Ondrejčáková, Vinoth Kumar Megraj Khandelwal, Slávka Čarnická, and Antigone Lazou. "Changes in PPAR gene expression and myocardial tolerance to ischaemia: relevance to pleiotropic effects of statinsThis article is one of a selection of papers published in a special issue on Advances in Cardiovascular Research." Canadian Journal of Physiology and Pharmacology 87, no. 12 (December 2009): 1028–36. http://dx.doi.org/10.1139/y09-071.

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Peroxisome proliferator-activated receptors (PPAR), which are key transcriptional regulators of lipid metabolism and energy production, have been suggested to play an important role in myocardial ischaemia–reperfusion (I/R) injury. Their role in cardioprotection, however, is not yet fully elucidated. Statins have shown beneficial effects on I/R damage beyond lipid lowering, and some of their cardioprotective cholesterol-independent effects may be related to the regulation of PPAR. To clarify this issue, we explored a potential link between a response to I/R and changes in cardiac PPARα protein and gene expression in simvastatin-treated normocholesterolaemic rats. After 5 days of treatment with simvastatin (10 mg/kg per day, p.o.), Langendorff-perfused hearts were subjected to 30 min regional ischaemia (occlusion of the left anterior descending coronary artery) or global ischaemia and 2 h reperfusion for the evaluation of the infarct size (triphenyltetrazolium chloride and planimetry; as percentage of risk area), ischaemic arrhythmias, and postischaemic contractile recovery. Baseline PPARα mRNA and protein levels were increased by 3-fold and 2-fold, respectively, in simvastatin-treated hearts compared with the untreated controls. Simvastatin-treated hearts exhibited smaller size of infarction (11.5% ± 0.4% vs. 33.7% ± 4% in controls; p < 0.01), improved postischaemic contractile recovery, and lower severity of arrhythmias during ischaemia and early reperfusion. Enhanced resistance to I/R injury was associated with preservation of mRNA and protein levels of PPARα in contrast to their marked downregulation in controls. In conclusion, statin-induced changes in the expression of PPARα may contribute to attenuation of myocardial I/R injury and thus suggest the involvement of cardioprotective mechanisms independent of inhibition of HMG-CoA reductase.
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Cabrera-Fuentes, Hector, Isabel Steinert, Klaus Preissner, Péter Bencsik, Márta Sárközy, Csaba Csonka, Péter Ferdinandy, et al. "Mechanism and consequences of the shift in cardiac arginine metabolism following ischaemia and reperfusion in rats." Thrombosis and Haemostasis 113, no. 03 (May 2015): 482–93. http://dx.doi.org/10.1160/th14-05-0477.

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SummaryCardiac ischaemia and reperfusion leads to irreversible injury and subsequent tissue remodelling. Initial reperfusion seems to shift arginine metabolism from nitric oxide (NO) to polyamine formation. This may limit functional recovery at reperfusion. The hypothesis was tested whether ischaemia/reperfusion translates such a shift in arginine metabolism in a tumour necrosis factor (TNF)-α-dependent way and renin-angiotensin system (RAS)-dependent way into a sustained effect. Both, the early post-ischaemic recovery and molecular adaptation to ischaemia/reperfusion were analysed in saline perfused rat hearts undergoing global no-flow ischaemia and reperfusion. Local TNF-α activation was blocked by inhibition of TNF-α sheddase ADAM17. To interfere with RAS captopril was administered. Arginase was inhibited by administration of Nor-NOHA. Long-term effects of ischemia/reperfusion on arginine metabolism were analysed in vivo in rats receiving an established ischaemia/reperfusion protocol in the closed chest mode. mRNA expression analysis indicated a shift in the arginine metabolism from NO formation to polyamine metabolism starting within 2 hours (h) of reperfusion and translated into protein expression within 24 h. Inhibition of the TNF-α pathway and captopril attenuated these delayed effects on post-ischaemic recovery. This shift in arginine metabolism was associated with functional impairment of hearts within 24 h. Inhibition of arginase but not that of TNF-α and RAS pathways improved functional recovery immediately. However, no benefit was observed after four months. In conclusion, this study identified TNF-α and RAS to be responsible for depressed cardiac function that occurred a few hours after reperfusion.
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Barrett, John A., Claudia K. Derian, Robert S. Swillo, Richard F. Woltmann, and Mark H. Perrone. "The role of the neutrophil and formed elements of the blood in anin vitromodel of reperfusion injury." Mediators of Inflammation 2, no. 1 (1993): 85–92. http://dx.doi.org/10.1155/s0962935193000122.

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Using The globally ischaemic isolated guinea-pig heart we conducted studies to assess the role of activated neutrophils (PMNs) and the role of the endothelium in reperfusion injury. Reperfusion injury was induced by a 20 min period of global ischaemia followed by a 30 min reperfusion with Krebs' buffer supplemented with f-Met–Leu–Phe (fMLP) and heparinized blood. Ischaemia alone or blood alone resulted in a complete recovery in contractile function measured by developed pressure, fMLP (500 μM) and blood, administered to normoxic hearts did not affect contractile function. The combination of 100 μM fMLP and blood beginning at reperfusion and continuing for 30 min decreased the recovery in contractile function (max. 33 ± 6% reovery) while buffer and 100 pM fMLP resulted in a complete recovery in function. In hearts infused with buffer and neutropenic blood incubated with 100 μM fMLP a complete recovery in function was observed. Isolated peritoneal neutrophils, 7–70 × 105PMN/ min, incubated with 100 μM fMLP and Krebs' solution decreased contractile function in a concentration-related manner (max. 44 ± 11% recovery). Platelets, plasma or red blood cells alone incubated with fMLP did not decrease recovery in developed pressure. Platelets and PMN incubated with 100 μM fMLP did not, while red blood cells and PMN did, elicit a reduction in recovery in contractile function (34 ± 4% recovery). A 20 min period of global ischaemia destroys the functional integrity of the endothelium (response to Ach). Pre-treatment of the heart with sufficient H2O2to functionally damage the endothelium, followed by infusion of Krebs' solution supplemented with blood and 100 μM fMLP also elicited a reduction in recovery of contractile function (42 ± 15% recovery). In summary, partially activated neutrophils play a major role in reperfusion injury and there exists a cooperativity between the RBC and PMN in this model.
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Masoud, Waleed G. T., Osama Abo Al-Rob, Yang Yang, Gary D. Lopaschuk, and Alexander S. Clanachan. "Tolerance to ischaemic injury in remodelled mouse hearts: less ischaemic glycogenolysis and preserved metabolic efficiency." Cardiovascular Research 107, no. 4 (July 6, 2015): 499–508. http://dx.doi.org/10.1093/cvr/cvv195.

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Hill, Bradford G., and Victor M. Darley-Usmar. "S-Nitrosation and thiol switching in the mitochondrion: a new paradigm for cardioprotection in ischaemic preconditioning." Biochemical Journal 412, no. 2 (May 14, 2008): e11-e13. http://dx.doi.org/10.1042/bj20080716.

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Understanding the molecular mechanisms through which the heart could be protected from ischaemic injury is of major interest and offers a potential route for the development of new therapies. Recently, several studies have uncovered intriguing relationships between nitric oxide-induced protein thiol modifications and the cardioprotected phenotype. In a highly cited, seminal article published in the Biochemical Journal in 2006, Burwell and colleagues addressed this issue and provided direct evidence for S-nitrosation of complex I of the mitochondrial electron transport chain. These authors were the first to show increased S-nitrosation of mitochondrial proteins from hearts subjected to the cardioprotective process known as ischaemic preconditioning. This study has paved the way for further investigations that collectively reveal a potential link between the mitochondrial S-nitrosoproteome and ischaemic preconditioning.
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Jin, Z. Q., J. S. Karliner, and D. A. Vessey. "Ischaemic postconditioning protects isolated mouse hearts against ischaemia/reperfusion injury via sphingosine kinase isoform-1 activation." Cardiovascular Research 79, no. 1 (March 18, 2008): 134–40. http://dx.doi.org/10.1093/cvr/cvn065.

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Cook, Alexandra, Stefan Engelhardt, and Metin Avkiran. "Paradoxical resistance to ischaemic injury in hearts of NHE1-transgenic mice." Journal of Molecular and Cellular Cardiology 42, no. 6 (June 2007): S196. http://dx.doi.org/10.1016/j.yjmcc.2007.03.595.

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Adameova, Adriana, Slavka Carnicka, Tomas Rajtik, Adrian Szobi, Martina Nemcekova, Pavel Svec, and Tana Ravingerova. "Upregulation of CaMKIIδ during ischaemia–reperfusion is associated with reperfusion-induced arrhythmias and mechanical dysfunction of the rat heart: involvement of sarcolemmal Ca2+-cycling proteins." Canadian Journal of Physiology and Pharmacology 90, no. 8 (August 2012): 1127–34. http://dx.doi.org/10.1139/y2012-019.

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Although Ca2+/calmodulin-dependent protein kinase II delta (CaMKIIδ) has been implicated in development of different phenotypes of myocardial ischaemia–reperfusion injury, its involvement in arrhythmogenesis and cardiac stunning is not sufficiently elucidated. Moreover, the mechanisms by which CaMKIIδ mediates disturbances in excitation–contraction coupling, are not exactly known. To investigate this, KN-93 (0.5 µmol/L), a CaMKII inhibitor, was administered before induction of global ischaemia and reperfusion in isolated Langendorff-perfused rat hearts. Expression of CaMKIIδ and the sarcollemal Ca2+-cycling proteins, known to be activated during reperfusion, was analyzed using immunoblotting. KN-93 reduced reperfusion-induced ectopic activity and the incidence of ventricular fibrillation. Likewise, the severity of arrhythmias was lower in KN-treated hearts. During the pre-ischaemia phase, neither inotropic nor chronotropic effects were elicited by KN-93, whereas post-ischaemic contractile recovery was significantly improved. Ischaemia–reperfusion increased the expression of CaMKIIδ and sodium–calcium exchanger (NCX1) proteins without any influence on the protein content of alpha 1c, a pore-forming subunit of L-type calcium channels (LTCCs). On the other hand, inhibition of CaMKII normalized changes in the expression of CaMKIIδ and NCX1. Taken together, CaMKIIδ seems to regulate its own turnover and to be an important component of cascade integrating NCX1, rather than LTCCs that promote ischaemia–reperfusion-induced contractile dysfunction and arrhythmias.
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Malakul, Wachirawadee, Kornkanok Ingkaninan, Pattara Sawasdee, and Owen L. Woodman. "The ethanolic extract of Kaempferia parviflora reduces ischaemic injury in rat isolated hearts." Journal of Ethnopharmacology 137, no. 1 (September 2011): 184–91. http://dx.doi.org/10.1016/j.jep.2011.05.004.

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Nadtochiy, Sergiy M., Andrew J. Tompkins, and Paul S. Brookes. "Different mechanisms of mitochondrial proton leak in ischaemia/reperfusion injury and preconditioning: implications for pathology and cardioprotection." Biochemical Journal 395, no. 3 (April 11, 2006): 611–18. http://dx.doi.org/10.1042/bj20051927.

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The mechanisms of mitochondrial proton (H+) leak under various pathophysiological conditions are poorly understood. In the present study it was hypothesized that different mechanisms underlie H+ leak in cardiac IR (ischaemia/reperfusion) injury and IPC (ischaemic preconditioning). Potential H+ leak mechanisms examined were UCPs (uncoupling proteins), allosteric activation of the ANT (adenine nucleotide translocase) by AMP, or the PT (permeability transition) pore. Mitochondria isolated from perfused rat hearts that were subjected to IPC exhibited a greater H+ leak than did controls (202±27%, P<0.005), and this increased leakage was completely abolished by the UCP inhibitor, GDP, or the ANT inhibitor, CAT (carboxyattractyloside). Mitochondria from hearts subjected to IR injury exhibited a much greater amount of H+ leak than did controls (411±28%, P<0.001). The increased leakage after IR was weakly inhibited by GDP, but was inhibited, >50%, by carboxyattractyloside. In addition, it was inhibited by cardioprotective treatment strategies including pre-IR perfusion with the PT pore inhibitors cyclosporin A or sanglifehrin A, the adenylate kinase inhibitor, AP5A (diadenosine pentaphosphate), or IPC. Together these data suggest that the small increase in H+ leak in IPC is mediated by UCPs, while the large increase in H+ leak in IR is mediated by the ANT. Furthermore, under all conditions studied, in situ myocardial O2 efficiency was correlated with isolated mitochondrial H+ leak (r2=0.71). In conclusion, these data suggest that the modulation of H+ leak may have important implications for the outcome of IR injury.
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Montgomery, J. A., M. Jetté, S. Huot, and C. Des Rosiers. "Acyloin production from aldehydes in the perfused rat heart: the potential role of pyruvate dehydrogenase." Biochemical Journal 294, no. 3 (September 15, 1993): 727–33. http://dx.doi.org/10.1042/bj2940727.

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Aldehydes represent an important class of cytotoxic products derived from free radical-induced lipid peroxidation which may contribute to reperfusion injury following myocardial infarct. Metabolism of aldehydes in the heart has not been well characterized aside from conjugation of unsaturated aldehydes with glutathione. However, aliphatic aldehydes like hexanal do not form stable glutathione conjugates. We have recently demonstrated in vitro that pig heart pyruvate dehydrogenase catalyses a reaction between pyruvate and saturated aldehydes to produce acyloins (3-hydroxyalkan-2-ones). In the present study, rat hearts were perfused with various aldehydes and pyruvate. Acyloins were generated from saturated aldehydes (butanal, hexanal or nonanal), but not from 2-hexanal (an unsaturated aldehyde) or malondialdehyde. Hearts perfused with 2 mM pyruvate and 10-100 microM hexanal rapidly took up hexanal in a dose-related manner (140-850 nmol/min), and released 3-hydroxyoctan-2-one (0.7-30 nmol/min), 2,3-octanediol (0-12 nmol/min) and hexanol (10-200 nmol/min). Small quantities of hexanoic acid (about 10 nmol/min) were also released. The rate of release of acyloin metabolites rose with increased concentration of hexanal, whereas hexanol release attained a plateau when hexanal infusion concentrations rose above 50 microM. Up to 50% of hexanal uptake could be accounted for by metabolite release. Less than 0.5% of hexanal uptake was found to be bound to acid-precipitable macromolecules. When hearts perfused with 50 microM hexanal and 2 mM pyruvate were subjected to a 15 min ischaemic period, the rates of release of 2,3-octanediol, 3-hydroxyoctan-2-one, hexanol and hexanoate during the reperfusion period were not significantly different from those in the pre-ischaemic period. Our results indicate that saturated aldehydes can be metabolically converted by the heart into stable diffusible compounds.
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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.

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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.
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Berlanga, Jorge, Danay Cibrian, Luis Guevara, Heberto Dominguez, Jose S. Alba, Alina Seralena, Gerardo Guillén, et al. "Growth-hormone-releasing peptide 6 (GHRP6) prevents oxidant cytotoxicity and reduces myocardial necrosis in a model of acute myocardial infarction." Clinical Science 112, no. 4 (January 17, 2007): 241–50. http://dx.doi.org/10.1042/cs20060103.

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Therapies aimed at enhancing cardiomyocyte survival following myocardial injury are urgently required. As GHRP6 [GH (growth hormone)-releasing peptide 6] has been shown to stimulate GH secretion and has beneficial cardiovascular effects, the aim of the present study was to determine whether GHRP6 administration reduces myocardial infarct size following acute coronary occlusion in vivo. Female Cuban Creole pigs were anaesthetized, monitored and instrumented to ensure a complete sudden left circumflex artery occlusion for 1 h, followed by a 72 h reperfusion/survival period. Animals were screened clinically before surgery and assigned randomly to receive either GHRP6 (400 μg/kg of body weight) or normal saline. Hearts were processed, and the area at risk and the infarct size were determined. CK-MB (creatine kinase MB) and CRP (C-reactive protein) levels and pathological Q-wave-affected leads were analysed and compared. Evaluation of the myocardial effect of GHRP6 also included quantitative histopathology, local IGF-I (insulin-growth factor-I) expression and oxidative stress markers. GHRP6 treatment did not have any influence on mortality during surgery associated with rhythm and conductance disturbances during ischaemia. Infarct mass and thickness were reduced by 78% and 50% respectively, by GHRP6 compared with saline (P<0.01). More than 50% of the GHRP6-treated pigs did not exhibit pathogological Q waves in any of the ECG leads. Quantitative histopathology and CK-MB and CRP serum levels confirmed the reduction in GHRP6-mediated necrosis (all P<0.05). Levels of oxidative stress markers suggested that GHRP6 prevented myocardial injury via a decrease in reactive oxygen species and by the preservation of antioxidant defence systems (all P<0.05). Myocardial IGF-I transcription was not amplified by GHRP6 treatment compared with the increase induced by the ischaemic episode in relation to expression in intact hearts (P<0.01). In conclusion, GHRP6 exhibits antioxidant effects which may partially contribute to reduce myocardial ischaemic damage.
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30

Oyagbemi, Ademola, Dirk Bester, Johan Esterhuyse, and Ebenezer Farombi. "Kolaviron and Garcinia kola Seed Extract Protect Against Ischaemia/Reperfusion Injury on Isolated Rat Heart." Drug Research 68, no. 05 (January 8, 2018): 286–95. http://dx.doi.org/10.1055/s-0043-123686.

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Abstract Background The incidence of cardiovascular diseases and its associated complications have increased greatly in the past three decades. The purpose of this study was to evaluate the acute cardioprotective effects of Garcinia kola (GK) seed extract and Kolaviron (KV) and determine mechanisms of action involving RISK signalling pathways. Methods Male Wistar rats were used in this study. Hearts were excised and mounted on the Langendorff perfusion system. The control, group 1 was perfused with dimethyl sulfoxide (DMSO), group II with KV and group III with GK respectively. Western blot analyses were performed on frozen heart tissues. Results Isolated rat hearts perfused with KV and GK attenuated apoptotic pathways with significant reduction in p38 MAPK protein phosphorylation, as well as reduction in total caspase 3, cleaved caspase 3 (Asp 175) and PARP cleavage. KV and GK also down-regulated p-JNK1 (Tyr 185) and p-JNK 2 (Thr 183) protein expression at the 10 min reperfusion time ponit. Cardioprotection was achieved in part, by enhancement of the reperfusion injury signalling kinase (RISK) pathway; as evidenced by significant increases in protein expresion of Akt/PKB and p-Akt/PKB (Ser 473) in KV and GK respectively. Conclusions KV and GK supplementation led to significant increases in the expressions of survival proteins. It is noteworthy that both KV and GK supplementation offered cardioprotection in ischaemic/reperfusion injury rat heart model. In all, GK showed better cardioprotective effect that KV.
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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.

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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.
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Choong, Y., J. Gavin, and D. Cottier. "Cardioplegic Protection of Hearts with Pre-Arrest Ischaemic Injury: Effect of Glucose, Aspartate, and Lactobionate." Thoracic and Cardiovascular Surgeon 43, no. 06 (December 1995): 331–37. http://dx.doi.org/10.1055/s-2007-1013805.

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33

Shimizu, Mikiko, Michael Tropak, Roberto J. Diaz, Fumiaki Suto, Harinee Surendra, Elena Kuzmin, Jing Li, et al. "Transient limb ischaemia remotely preconditions through a humoral mechanism acting directly on the myocardium: evidence suggesting cross-species protection." Clinical Science 117, no. 5 (August 3, 2009): 191–200. http://dx.doi.org/10.1042/cs20080523.

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rIPC (remote ischaemic preconditioning) is a phenomenon whereby short periods of ischaemia and reperfusion of a tissue or organ (e.g. mesentery, kidney) can protect a distant tissue or organ (e.g. heart) against subsequent, potentially lethal, ischaemia. We, and others, have shown that transient limb ischaemia can provide potent myocardial protection experimentally and clinically during cardiac surgery. Nonetheless, our understanding of the signal transduction from remote stimulus to local effect remains incomplete. The aim of the present study was to define the humoral nature of rIPC effector(s) from limb ischaemia and to study their local effects in isolated heart and cardiomyocyte models. Using a Langendorff preparation, we show that infarct size after coronary artery ligation and reperfusion was substantially reduced by rIPC in vivo, this stimulus up-regulating the MAPKs (mitogen-activating protein kinases) p42/p44, and inducing PKCε (protein kinase Cε) subcellular redistribution. Pre-treatment with the plasma and dialysate of plasma (obtained using 15 kDa cut-off dialysis membrane) from donor rabbits subjected to rIPC similarly protected against infarction. The effectiveness of the rIPC dialysate was abrogated by passage through a C18 hydrophobic column, but eluate from this column provided the same level of protection. The dialysate of rIPC plasma from rabbits and humans was also tested in an isolated fresh cardiomyocyte model of simulated ischaemia and reperfusion. Necrosis in cardiomyocytes treated with rIPC dialysate was substantially reduced compared with control, and was similar to cells pre-treated by ‘classical’ preconditioning. This effect, by rabbit rIPC dialysate, was blocked by pre-treatment with the opiate receptor blocker naloxone. In conclusion, in vivo transient limb ischaemia releases a low-molecular-mass (<15 kDa) hydrophobic circulating factor(s) which induce(s) a potent protection against myocardial ischaemia/reperfusion injury in Langendorff-perfused hearts and isolated cardiomyocytes in the same species. This cardioprotection is transferable across species, independent of local neurogenic activity, and requires opioid receptor activation.
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EDLUND, A., K. SAHLIN, and A. WENNMALM. "Effect of prostacyclin on the severity of ischaemic injury in rabbit hearts subjected to coronary ligation." Journal of Molecular and Cellular Cardiology 18, no. 10 (October 1986): 1067–76. http://dx.doi.org/10.1016/s0022-2828(86)80293-0.

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35

Kawakami, T., C. Löwbeer, G. Valen, and J. Vaage. "Mechanical conversion of post-ischaemic ventricular fibrillation: effects on function and myocyte injury in isolated rat hearts." Scandinavian Journal of Clinical and Laboratory Investigation 59, no. 1 (January 1999): 9–16. http://dx.doi.org/10.1080/00365519950185959.

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36

Bhimji, S., D. V. Godin, and J. H. McNeill. "Coronary artery ligation and reperfusion in rabbits made diabetic with alloxan." Journal of Endocrinology 112, no. 1 (January 1987): 43–49. http://dx.doi.org/10.1677/joe.0.1120043.

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ABSTRACT The biochemical and functional changes associated with ligation (40 min) of the left circumflex coronary artery and subsequent reperfusion (60 min) in the rabbit made diabetic with alloxan were studied and compared with those of control animals. Measurement of haemodynamic parameters revealed that both left ventricular pressure and mean arterial pressure were significantly (P < 0·05) decreased after ligation and reperfusion in the diabetic animals compared with controls. Analysis of subcellular organelle enzyme markers from the ischaemic tissue revealed that sarcolemmal Na+,K+-ATPase, mitochondrial ATPase and sarcoplasmic reticulum ATPase activities were decreased after ligation to the same extent in the diabetic and control animals. However, upon reperfusion, the recovery of mitochondrial ATPase activity was significantly (P < 0·05) less in the diabetic animals than in the controls. Ion measurements revealed a significant (P < 0·05) depletion of Mg in diabetic hearts before ligation, and this was augmented during reperfusion. In contrast, a significantly (P < 0·05) higher calcium accumulation was observed upon reperfusion in the hearts of diabetic animals. Similarly, both tissue ATP levels and the ability of the mitochondria to generate ATP were depressed to a greater degree in the diabetic animals. Our results indicate, therefore, a greater susceptibility of the diabetic myocardium to ischaemic/reperfusion injury which in the clinical situation would exacerbate the problems associated with atherosclerosis and possibly contribute to the high mortality from cardiovascular complications in diabetic patients. J. Endocr. (1987) 112, 43–49
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Halestrap, A. P., E. Doran, J. P. Gillespie, and A. O'Toole. "Mitochondria and cell death." Biochemical Society Transactions 28, no. 2 (February 1, 2000): 170–77. http://dx.doi.org/10.1042/bst0280170.

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Mitochondria play a central role in both apoptosis and necrosis through the opening of the mitochondrial permeability transition pore (MPTP). This is thought to be formed through a Ca2+-triggered conformational change of the adenine nucleotide translocase (ANT) bound to matrix cyclophilin-D and we have now demonstrated this directly by reconstitution of the pure components. Opening of the MPTP causes swelling and uncoupling of mitochondria which, unrestrained, leads to necrosis. In ischaemia/reperfusion injury of the heart we have shown MPTP opening directly. Recovery of hearts correlates with subsequent closure, and agents that prevent opening or enhance closure protect from injury. Transient MPTP opening may also be involved in apoptosis by initially causing swelling and rupture of the outer membrane to release cytochrome c (cyt c), which then activates the caspase cascade and sets apoptosis in motion. Subsequent MPTP closure allows ATP levels to be maintained, ensuring that cell death remains apoptotic rather than necrotic. Apoptosis in the hippocampus that occurs after a hypoglycaemic or ischaemic insult is triggered by this means. Other apoptotic stimuli such as cytokines or removal of growth factors also involve mitochondrial cyt c release, but here there is controversy over whether the MPTP is involved. In many cases cyt c release is seen without any mitochondrial depolarization, suggesting that the MPTP does not open. Recent data of our own and others have revealed a specific outer-membrane cyt c-release pathway involving porin that does not release other intermembrane proteins such as adenylate kinase. This is opened by pro-apototic members of the Bcl-2 family such as BAX and prevented by anti-apoptotic members such as Bcl-xL. Our own data suggest that this pathway may interact directly with the ANT in the inner membrane at contact sites.
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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.

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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.
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39

Churchill, E. N., and D. Mochly-Rosen. "The roles of PKCδ and ϵ isoenzymes in the regulation of myocardial ischaemia/reperfusion injury." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1040–42. http://dx.doi.org/10.1042/bst0351040.

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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.
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Lunder, Mojca, Miodrag Janić, Lovro Žiberna, Gorazd Drevenšek, and Mišo Šabovič. "A low-dose atorvastatin and losartan combination directly improves aortic ring relaxation and diminishes ischaemic-reperfusion injury in isolated rat hearts." Medical Science Monitor 18, no. 9 (2012): BR366—BR374. http://dx.doi.org/10.12659/msm.883347.

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KUPATT, C. "2532 Endothelial nitric oxide synthase activation by vascular endothelial growth factor or hsp90 decreases post-ischaemic reperfusion injury in pig hearts." European Heart Journal 24, no. 5 (March 2003): 476. http://dx.doi.org/10.1016/s0195-668x(03)95404-2.

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42

BRUNVAND, H., L. FRØYLAND, J. WESTBY, E. HEXEBERG, R. K. BERGE, and K. GRONG. "Peroxisomal fatty acid oxidation capacity is more resistant to ischaemic and reperfusion injury than mitochondrial fatty acid oxidation capacity in feline hearts." Acta Physiologica Scandinavica 157, no. 2 (June 1996): 133–45. http://dx.doi.org/10.1046/j.1365-201x.1996.498243000.x.

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43

Piuhola, Jarkko, Risto Kerkelä, Jacqueline I. Keenan, Mark B. Hampton, A. Mark Richards, and Chris J. Pemberton. "Direct cardiac actions of erythropoietin (EPO): effects on cardiac contractility, BNP secretion and ischaemia/reperfusion injury." Clinical Science 114, no. 4 (January 15, 2008): 293–304. http://dx.doi.org/10.1042/cs20070229.

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EPO (erythropoietin) has recently been shown to have protective actions upon the myocardium; however, the direct effects of EPO upon cardiac contractile and secretory functions are unknown and the signalling mechanisms are not well defined. In the present study, we provide the first evidence of direct cardiac contractile actions of EPO. In isolated perfused Sprague–Dawley rat hearts, a 30 min infusion of EPO significantly increased contractility in a dose-dependent fashion (maximal change 18±2% with 1 unit/ml EPO; P<0.005 compared with vehicle). Perfusate ET-1 (endothelin-1) increased transiently during EPO infusion, and the ETA/ETB antagonist bosentan abolished the inotropic response to EPO. BNP (B-type natriuretic peptide) secretion (28±8%; P<0.05) and nuclear transcription factor GATA-4 DNA-binding activity (51%; P<0.05) were both significantly increased by EPO and blocked by bosentan. In a model of global ischaemic injury, delivery of 1 unit/ml EPO during reperfusion significantly attenuated creatine kinase release (28±12%; P<0.05) and significantly improved contractile recovery (P<0.001), independent of ETA blockade. Apoptotic indices [assessed by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling)/cleaved caspase-3-positive cells] were significantly decreased (P<0.01) by 1 unit/ml EPO during reperfusion alone, coincident with significantly increased phosphorylation of myocardial JAK2 (Janus kinase 2) and STAT3 (signal transducer and activator of transcription 3). Thus EPO directly enhances cardiac contractility and BNP secretion and alleviates ischemia/reperfusion injury via ET-1-dependent and -independent mechanisms respectively.
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Devereaux, P. J., and Wojciech Szczeklik. "Myocardial injury after non-cardiac surgery: diagnosis and management." European Heart Journal 41, no. 32 (May 16, 2019): 3083–91. http://dx.doi.org/10.1093/eurheartj/ehz301.

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Abstract Myocardial injury after non-cardiac surgery (MINS) is due to myocardial ischaemia (i.e. supply-demand mismatch or thrombus) and is associated with an increased risk of mortality and major vascular complications at 30 days and up to 2 years after non-cardiac surgery. The diagnostic criteria for MINS includes an elevated post-operative troponin measurement judged as resulting from myocardial ischaemia (i.e. no evidence of a non-ischaemic aetiology), during or within 30 days after non-cardiac surgery, and without the requirement of an ischaemic feature (e.g. ischaemic symptom, ischaemic electrocardiography finding). For patients with MINS who are not at high risk of bleeding, physicians should consider initiating dabigatran 110 mg twice daily and low-dose aspirin. Physicians should also consider initiating statin therapy in patients with MINS. Most MINS patients should only be referred to cardiac catheterization if they demonstrate recurrent instability (e.g. cardiac ischaemia, heart failure). Patients ≥65 years of age or with known atherosclerotic disease should have troponin measurements on days 1, 2, and 3 after surgery while the patient is in hospital to avoid missing &gt;90% of MINS and the opportunity to initiate secondary prophylactic measures and follow-up.
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45

Pipicz, Márton, Virág Demján, Márta Sárközy, and Tamás Csont. "Effects of Cardiovascular Risk Factors on Cardiac STAT3." International Journal of Molecular Sciences 19, no. 11 (November 12, 2018): 3572. http://dx.doi.org/10.3390/ijms19113572.

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Nuclear, mitochondrial and cytoplasmic signal transducer and activator of transcription 3 (STAT3) regulates many cellular processes, e.g., the transcription or opening of mitochondrial permeability transition pore, and its activity depends on the phosphorylation of Tyr705 and/or Ser727 sites. In the heterogeneous network of cardiac cells, STAT3 promotes cardiac muscle differentiation, vascular element formation and extracellular matrix homeostasis. Overwhelming evidence suggests that STAT3 is beneficial for the heart, plays a role in the prevention of age-related and postpartum heart failure, protects the heart against cardiotoxic doxorubicin or ischaemia/reperfusion injury, and is involved in many cardioprotective strategies (e.g., ischaemic preconditioning, perconditioning, postconditioning, remote or pharmacological conditioning). Ischaemic heart disease is still the leading cause of death worldwide, and many cardiovascular risk factors contribute to the development of the disease. This review focuses on the effects of various cardiovascular risk factors (diabetes, aging, obesity, smoking, alcohol, depression, gender, comedications) on cardiac STAT3 under non-ischaemic baseline conditions, and in settings of ischaemia/reperfusion injury with or without cardioprotective strategies.
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46

Solaini, Giancarlo, and David A. Harris. "Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion." Biochemical Journal 390, no. 2 (August 23, 2005): 377–94. http://dx.doi.org/10.1042/bj20042006.

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Heart tissue is remarkably sensitive to oxygen deprivation. Although heart cells, like those of most tissues, rapidly adapt to anoxic conditions, relatively short periods of ischaemia and subsequent reperfusion lead to extensive tissue death during cardiac infarction. Heart tissue is not readily regenerated, and permanent heart damage is the result. Although mitochondria maintain normal heart function by providing virtually all of the heart's ATP, they are also implicated in the development of ischaemic damage. While mitochondria do provide some mechanisms that protect against ischaemic damage (such as an endogenous inhibitor of the F1Fo-ATPase and antioxidant enzymes), they also possess a range of elements that exacerbate it, including ROS (reactive oxygen species) generators, the mitochondrial permeability transition pore, and their ability to release apoptotic factors. This review considers the process of ischaemic damage from a mitochondrial viewpoint. It considers ischaemic changes in the inner membrane complexes I–V, and how this might affect formation of ROS and high-energy phosphate production/degradation. We discuss the contribution of various mitochondrial cation channels to ionic imbalances which seem to be a major cause of reperfusion injury. The different roles of the H+, Ca2+ and the various K+ channel transporters are considered, particularly the K+ATP (ATP-dependent K+) channels. A possible role for the mitochondrial permeability transition pore in ischaemic damage is assessed. Finally, we summarize the metabolic and pharmacological interventions that have been used to alleviate the effects of ischaemic injury, highlighting the value of these or related interventions in possible therapeutics.
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47

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.

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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.
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48

Ho, Choon-Kiat, Chee-Wei Lee, Jian Lu, Jian Wu, Woon-Puay Koh, Chung-Yip Chan, Shervanthi Homer-Vanniasinkam, and Alexandre KH Chao. "New Hope for an Old Cure: A Pilot Animal Study on Selective Venesection in Attenuating the Systemic Effects of Ischaemic-Reperfusion Injury." Annals of the Academy of Medicine, Singapore 38, no. 7 (July 15, 2009): 569–75. http://dx.doi.org/10.47102/annals-acadmedsg.v38n7p569.

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Introduction: Reperfusion of acutely ischaemic tissue may, paradoxically, lead to systemic complications. This phenomenon is believed to be initiated by humoral factors that have accumulated in the ischaemic tissue. The ancient art of venesection may reduce the load of these mediators at the point of reperfusion. The aim of this study is to test if selective venesection, by removing the initial venous return from the ischaemic tissue, can attenuate the systemic effects of the ischaemic-reperfusion injury using a porcine model of acute limb ischaemia. Materials and Methods: The right femoral arteries of anaesthetised female pigs were clamped. Twelve pigs were divided into 2 groups (n = 6 per group). In the treatment group, 5% of blood volume was venesected from the ipsilateral femoral vein upon reperfusion; the other arm served as control. The animals were sacrificed after 4 days for histological examination. A pathologist, blinded to the experimental groups, graded the degree of microscopic injury. Results: For the control group, the kidneys showed glomeruli and tubular damage. The livers demonstrated architectural distortion with cellular oedema. There was pulmonary oedema as well as extensive capillary congestion and neutrophil infiltration. Such findings were absent or reduced in the venesected animals. Consequently, the injury scores for the kidney, lung, liver and heart were significantly less for the venesected animals. Conclusion: Selective venesection reduces the remote organ injuries of the ischaemic-reperfusion phenomenon. Key words: Acute ischaemia, Humoral factors, MODS, Pulmonary oedema
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49

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.

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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.
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Corno, Antonio, Roberto Motterlini, Laura Brenna, Francesco Santoro, and Michele Samaja. "Ischaemia/reperfusion in the posthypoxaemic re-oxygenated myocardium: haemodynamic study in the isolated perfused rat heart." Perfusion 8, no. 1 (January 1993): 113–18. http://dx.doi.org/10.1177/026765919300800115.

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In order to study the haemodynamics of reperfusion injury in the post hypoxaemic heart, we exposed buffer-perfused isolated rat hearts to either: (1) 20-minute low-flow ischaemia or (2) 20-minute hypoxaemia followed by re-oxygenation and further ischaemia/reperfusion. In group 2, the myocardial contractility recovered less (p <0.002) than in group 1. This model therefore represents with sufficient reliability the clinical situation where hypoxaemic hearts are re-oxgenated before ischaemia/reperfusion and receive more severe injury than hearts exposed to ischaemia/reperfusion only. To locate the major site of the injury, further data were obtained (1) with infusion of superoxide dismutase and catalase during hypoxaemia and in the first five minutes of re-oxygenation, and (2) by eliminating re-oxygenation. It appears that the major determinant of reperfusion injury in hypoxaemic hearts is to be looked for in the events underlying hypoxaemia or re-oxygenation, and is mediated by oxygen- derived free radicals.
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