Academic literature on the topic 'Ischemia and reperfusion injury, Creatine/metabolism'
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Journal articles on the topic "Ischemia and reperfusion injury, Creatine/metabolism"
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Tian, Fang, Runzhe Liu, Chaoxin Fan, Yi Sun, Xi Huang, Zongxiu Nie, Xin Zhao, and Xiaoping Pu. "Effects of Thymoquinone on Small-Molecule Metabolites in a Rat Model of Cerebral Ischemia Reperfusion Injury Assessed using MALDI-MSI." Metabolites 10, no. 1 (January 7, 2020): 27. http://dx.doi.org/10.3390/metabo10010027.
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Thymoquinone is one of the main components present in Nigella sativa seeds and is known to have various biological functions in inflammation, oxidative stress, tumors, aging, and in lowering blood glucose levels. Few studies have focused on its neuroprotective effects and its regulation of small-molecule metabolites during cerebral ischemia reperfusion injury. In this study, transient middle cerebral occlusion (tMCAO) was used to establish the rat model of cerebral ischemia reperfusion injury. We investigated the effects of thymoquinone using matrix-assisted laser desorption ionization mass spectrometry imaging (MALDI-MSI) in a model of ischemia reperfusion injury to explore the changes in small-molecule metabolites in the brain. We found that that thymoquinone significantly improved neurobehavioral scores, reduced the cerebral infarct area, alleviated brain edema, and increased the number of normal neurons following injury. MALDI-MSI revealed that thymoquinone reduced abnormal accumulations of glucose, citric acid, succinate and potassium ions. Thymoquinone also increased the amount of energy-related molecules such as ADP, AMP, GMP, and creatine, antioxidants such as glutathione, ascorbic acid, and taurine, and other metabolism-related molecules such as glutamate, glutamine, aspartate, N-acetyl-L-aspartate, and sodium ions in damaged areas of the brain following cerebral ischemia reperfusion injury. In summary, based on the neuroprotective effect of thymoquinone on cerebral ischemia reperfusion injury, this study revealed the regulation of thymoquinone on energy metabolism and small-molecule substance metabolism.
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Sandhu, G. S., A. C. Burrier, and D. R. Janero. "Adenosine deaminase inhibitors attenuate ischemic injury and preserve energy balance in isolated guinea pig heart." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1249—H1256. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1249.
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We investigated the effect of the adenosine deaminase inhibitors erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) and coformycin on high-energy phosphate metabolism, tissue nucleotides and nucleosides, and recovery of contractile function in isolated, perfused guinea pig hearts. EHNA and coformycin (10 microM) improved postischemic recovery of contractile function approximately 85% and enhanced coronary flow rate in reperfused tissue approximately 40%. The protective effect of EHNA on recovery of contractile function was concentration dependent. Although adenosine (10 microM) increased coronary flow rate on reperfusion approximately twofold over vehicle, it failed to improve postischemic recovery of contractile function. EHNA and coformycin preserved cardiac ATP levels and increased endogenous tissue adenosine during ischemia. During reperfusion, these agents enhanced recovery of high-energy phosphates approximately twofold and potentiated adenosine release into the perfusate with concentration dependency. Furthermore, EHNA and coformycin reduced the extent of myocardial ischemia-reperfusion injury, as indicated by the approximately 55% reduction in creatine phosphokinase release. We conclude that inhibitors of adenosine deaminase attenuate myocardial ischemic injury and improve postischemic recovery of contractile function and metabolism through endogenous myocardial adenosine enhancement and ATP preservation.
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Spindler, Matthias, Klaus Meyer, Hinrik Strömer, Andrea Leupold, Ernest Boehm, Helga Wagner, and Stefan Neubauer. "Creatine kinase-deficient hearts exhibit increased susceptibility to ischemia-reperfusion injury and impaired calcium homeostasis." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 3 (September 2004): H1039—H1045. http://dx.doi.org/10.1152/ajpheart.01016.2003.
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The creatine kinase (CK) system is involved in the rapid transport of high-energy phosphates from the mitochondria to the sites of maximal energy requirements such as myofibrils and sarcolemmal ion pumps. Hearts of mice with a combined knockout of cytosolic M-CK and mitochondrial CK (M/Mito-CK−/−) show unchanged basal left ventricular (LV) performance but reduced myocardial high-energy phosphate concentrations. Moreover, skeletal muscle from M/Mito-CK−/− mice demonstrates altered Ca2+ homeostasis. Our hypothesis was that in CK-deficient hearts, a cardiac phenotype can be unmasked during acute stress conditions and that susceptibility to ischemia-reperfusion injury is increased because of altered Ca2+ homeostasis. We simultaneously studied LV performance and myocardial Ca2+ metabolism in isolated, perfused hearts of M/Mito-CK−/− ( n = 6) and wild-type (WT, n = 8) mice during baseline, 20 min of no-flow ischemia, and recovery. Whereas LV performance was not different during baseline conditions, LV contracture during ischemia developed significantly earlier (408 ± 72 vs. 678 ± 54 s) and to a greater extent (50 ± 2 vs. 36 ± 3 mmHg) in M/Mito-CK−/− mice. During reperfusion, recovery of diastolic function was impaired (LV end-diastolic pressure: 22 ± 3 vs. 10 ± 2 mmHg), whereas recovery of systolic performance was delayed, in M/Mito-CK−/− mice. In parallel, Ca2+ transients were similar during baseline conditions; however, M/Mito-CK−/− mice showed a greater increase in diastolic Ca2+ concentration ([Ca2+]) during ischemia (237 ± 54% vs. 167 ± 25% of basal [Ca2+]) compared with WT mice. In conclusion, CK-deficient hearts show an increased susceptibility of LV performance and Ca2+ homeostasis to ischemic injury, associated with a blunted postischemic recovery. This demonstrates a key function of an intact CK system for maintenance of Ca2+ homeostasis and LV mechanics under metabolic stress conditions.
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Ji, Lele, Feng Fu, Lihua Zhang, Wenchong Liu, Xiaoqing Cai, Lei Zhang, Qiangsun Zheng, Haifeng Zhang, and Feng Gao. "Insulin attenuates myocardial ischemia/reperfusion injury via reducing oxidative/nitrative stress." American Journal of Physiology-Endocrinology and Metabolism 298, no. 4 (April 2010): E871—E880. http://dx.doi.org/10.1152/ajpendo.00623.2009.
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It is well known that insulin possesses a cardioprotective effect and that insulin resistance is closely related to cardiovascular diseases. Peroxynitrite (ONOO−) formation may trigger oxidative/nitrative stress and represent a major cytotoxic effect in heart diseases. This study was designed to investigate whether insulin attenuates ONOO− generation and oxidative/nitrative stress in acute myocardial ischemia/reperfusion (MI/R). Adult male rats were subjected to 30 min of myocardial ischemia and 3 h of reperfusion. Rats randomly received vehicle, insulin, or insulin plus wortmannin. Arterial blood pressure and left ventricular pressure were monitored throughout the experiment. Insulin significantly improved cardiac functions and reduced myocardial infarction, apoptotic cell death, and blood creatine kinase/lactate dehydrogenase levels following MI/R. Myocardial ONOO− formation was significantly attenuated after insulin treatment. Moreover, insulin resulted in a significant increase in Akt and endothelial nitric oxide (NO) synthase (eNOS) phosphorylation, NO production, and antioxidant capacity in ischemic/reperfused myocardial tissue. On the other hand, insulin markedly reduced MI/R-induced inducible NOS (iNOS) and gp91phox expression in cardiac tissue. Inhibition of insulin signaling with wortmannin not only blocked the cardioprotection of insulin but also markedly attenuated insulin-induced antioxidative/antinitrative effect. Furthermore, the suppression on ONOO− formation by either insulin or an ONOO− scavenger uric acid reduced myocardial infarct size in rats subjected to MI/R. We concluded that insulin exerts a cardioprotective effect against MI/R injury by blocking ONOO− formation. Increased physiological NO production (via eNOS phosphorylation) and superoxide anion reduction contribute to the antioxidative/antinitrative effect of insulin, which can be reversed by inhibiting phosphatidylinositol 3′-kinase. These results provide important novel information on the mechanisms of cardiovascular actions of insulin.
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Yoshino, Takuya, Tomohisa Nagoshi, Ryuko Anzawa, Yusuke Kashiwagi, Keiichi Ito, Daisuke Katoh, Masami Fujisaki, et al. "Preconditioning actions of aldosterone through p38 signaling modulation in isolated rat hearts." Journal of Endocrinology 222, no. 2 (June 3, 2014): 289–99. http://dx.doi.org/10.1530/joe-14-0067.
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Although persistent excessive actions of aldosterone have unfavorable effects on the cardiovascular system, primarily via mineralocorticoid receptor (MR)-dependent pathways, the pathophysiological significance of aldosterone cascade activation in heart diseases has not yet been fully clarified. We herein examined the effects of short-term aldosterone stimulation at a physiological dose on cardiac function during ischemia–reperfusion injury (IRI). In order to study the effects of aldosterone preconditioning, male Wistar rat Langendorff hearts were perfused with 10−9 mol/l of aldosterone for 10 min before ischemia, and the response to IRI was assessed. Although aldosterone did not affect the baseline hemodynamic parameters, preconditioning actions of aldosterone significantly improved the recovery in left ventricular contractility and left ventricular end-diastolic pressure associated with a reduced activity of creatine phosphokinase released into the perfusate after ischemia–reperfusion. Notably, the MR inhibitor eplerenone did not abrogate these beneficial effects. Biochemical analyses revealed that p38MAPK phosphorylation was significantly increased during aldosterone preconditioning before ischemia, whereas its phosphorylation was substantially attenuated during sustained ischemia–reperfusion, compared with the results for in the non-preconditioned control hearts. This dual regulation of p38MAPK was not affected by eplerenone. The phosphorylation levels of other MAPKs were not altered by aldosterone preconditioning. In conclusion, the temporal induction of the aldosterone cascade, at a physiological dose, has favorable effects on cardiac functional recovery and injury following ischemia–reperfusion in a MR-independent manner. Phasic dynamism of p38MAPK activation may play a key role in the physiological compensatory pathway of aldosterone under severe cardiac pathological conditions.
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Yoshida, Shinichi, Raul Busto, Elena Martinez, Peritz Scheinberg, and Myron D. Ginsberg. "Regional Brain Energy Metabolism after Complete versus Incomplete Ischemia in the Rat in the Absence of Severe Lactic Acidosis." Journal of Cerebral Blood Flow & Metabolism 5, no. 4 (December 1985): 490–501. http://dx.doi.org/10.1038/jcbfm.1985.75.
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Levels of energy metabolites were measured in forebrain regions in fasted rats subjected to 4-h recirculation after 1 h of either incomplete or complete ischemia. Both models of ischemia were produced by a procedure combining bilateral common carotid artery occlusion, systemic hypotension, and CSF pressure elevation; the degree of intracranial hypertension was varied to produce incomplete and complete ischemia. Levels of brain lactate at the end of ischemia ranged from 16 to 19 mmol/ kg in incomplete ischemia and from 11 to 13 mmol/kg in complete ischemia. Energy metabolism recovered evenly in the neocortical and subcortical regions with recirculation after incomplete ischemia. The metabolic recovery in the cerebral cortex after complete ischemia was similar to that observed after incomplete ischemia; however, recovery in the subcortical regions after complete ischemia was less extensive, NADH fluorescence remained high, and there was a fall in total creatine. Intracellular pH in the dorsal thalamus was more alkalotic after complete than incomplete ischemia. Thus, in the absence of profound tissue lactic acidosis, residual CBF during prolonged ischemia helps postischemic restitution of brain energy metabolism in subcortical regions. The pattern of poor recovery in these regions after complete ischemia suggests inadequate reperfusion. The decreased total creatine and the severe tissue alkalosis may be biochemical markers of advanced tissue injury during reflow.
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Karu, Inga, Peeter Tähepöld, Toomas Andres Sulling, Margus Alver, Mihkel Zilmer, and Joel Starkopf. "Off-Pump Coronary Surgery causes Immediate Release of Myocardial Damage Markers." Asian Cardiovascular and Thoracic Annals 17, no. 5 (October 2009): 494–99. http://dx.doi.org/10.1177/0218492309348637.
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Off-pump coronary surgery does not eliminate the risks of ischemia-reperfusion injury. The main objective of this study was to describe the extent and time course of changes in myocardial metabolism and development of myocardial injury associated with revascularization. Coronary sinus and arterial blood samples for measurement of troponin I, creatine kinase MB, lactate, glutathione, and interleukin-6 were taken from 23 patients prior to grafting, after completion of each anastomosis, and up to the 1st postoperative morning. The results were evaluated together with parameters of cardiac function. Release of lactate, creatinine kinase MB, and troponin I into the coronary sinus was evident after completion of the 1st graft, and increased over time. During the procedure, only trace amounts of oxidized and reduced glutathione were detected in coronary sinus and arterial blood. Significant increases in interleukin-6 were found in coronary sinus samples after 5 and 20 min of reperfusion. Surgical trauma during off-pump coronary surgery is sufficient to activate an inflammatory response in the myocardium, together with unfavorable metabolic conditions to cause myocardial necrosis.
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Castillo, Oscar Arriagada, Gustavo Herrera, Carlos Manriquez, Andrea F. Rojas, and Daniel R. González. "Pharmacological Inhibition of S-Nitrosoglutathione Reductase Reduces Cardiac Damage Induced by Ischemia–Reperfusion." Antioxidants 10, no. 4 (April 2, 2021): 555. http://dx.doi.org/10.3390/antiox10040555.
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The cardioprotective effects of nitric oxide (NO) have been described through S-nitrosylation of several important proteins in the mitochondria of the cardiomyocyte. S-nitrosoglutathione reductase (GSNOR) is an enzyme involved in the metabolism of S-nitrosothiols by producing denitrosylation, thus limiting the cardioprotective effect of NO. The effect of GSNOR inhibition on the damage by cardiac ischemia–reperfusion is still unclear. We tested the hypothesis that pharmacological inhibition of GSNOR promotes cardioprotection by increasing the levels of protein S-nitrosylation. In a model of ischemia–reperfusion in isolated rat heart, the effect of a GSNOR inhibitor, 5-chloro-3-(2-[4-ethoxyphenyl) (ethyl) amino]-2-oxoethyl)-1H-indole-2-carboxylic acid (C2), was investigated. Ventricular function and hemodynamics were determined, in addition to tissue damage and S-nitrosylation of mitochondrial proteins. Hearts treated with C2 showed a lower release of myocardial damage marker creatine kinase and a reduction in the infarcted area. It also improved post-ischemia ventricular function compared to controls. These results were associated with increasing protein S-nitrosylation, specifically of the mitochondrial complexes III and V. The pharmacological inhibition of GSNOR showed a concentration-dependent cardioprotective effect, being observed in functional parameters and myocardial damage, which was maximal at 1 µmol/L, associated with increased S-nitrosylation of mitochondrial proteins. These data suggest that GSNOR is an interesting pharmacological target for cardiac reperfusion injury.
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Aoyagi, Toshinori, Jason K. Higa, Hiroko Aoyagi, Naaiko Yorichika, Briana K. Shimada, and Takashi Matsui. "Cardiac mTOR rescues the detrimental effects of diet-induced obesity in the heart after ischemia-reperfusion." American Journal of Physiology-Heart and Circulatory Physiology 308, no. 12 (June 15, 2015): H1530—H1539. http://dx.doi.org/10.1152/ajpheart.00008.2015.
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Diet-induced obesity deteriorates the recovery of cardiac function after ischemia-reperfusion (I/R) injury. While mechanistic target of rapamycin (mTOR) is a key mediator of energy metabolism, the effects of cardiac mTOR in ischemic injury under metabolic syndrome remains undefined. Using cardiac-specific transgenic mice overexpressing mTOR (mTOR-Tg mice), we studied the effect of mTOR on cardiac function in both ex vivo and in vivo models of I/R injury in high-fat diet (HFD)-induced obese mice. mTOR-Tg and wild-type (WT) mice were fed a HFD (60% fat by calories) for 12 wk. Glucose intolerance and insulin resistance induced by the HFD were comparable between WT HFD-fed and mTOR-Tg HFD-fed mice. Functional recovery after I/R in the ex vivo Langendorff perfusion model was significantly lower in HFD-fed mice than normal chow diet-fed mice. mTOR-Tg mice demonstrated better cardiac function recovery and had less of the necrotic markers creatine kinase and lactate dehydrogenase in both feeding conditions. Additionally, mTOR overexpression suppressed expression of proinflammatory cytokines, including IL-6 and TNF-α, in both feeding conditions after I/R injury. In vivo I/R models showed that at 1 wk after I/R, HFD-fed mice exhibited worse cardiac function and larger myocardial scarring along myofibers compared with normal chow diet-fed mice. In both feeding conditions, mTOR overexpression preserved cardiac function and prevented myocardial scarring. These findings suggest that cardiac mTOR overexpression is sufficient to prevent the detrimental effects of diet-induced obesity on the heart after I/R, by reducing cardiac dysfunction and myocardial scarring.
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Jiang, Miaomiao, Jingyu Ni, Yuanlin Cao, Xiaoxue Xing, Qian Wu, and Guanwei Fan. "Astragaloside IV Attenuates Myocardial Ischemia-Reperfusion Injury from Oxidative Stress by Regulating Succinate, Lysophospholipid Metabolism, and ROS Scavenging System." Oxidative Medicine and Cellular Longevity 2019 (June 24, 2019): 1–17. http://dx.doi.org/10.1155/2019/9137654.
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Astragaloside IV is one of the main active ingredients isolated from Astragalus membranaceus. Here we confirmed its protective effect against cardiac ischemia-reperfusion (I/R) injury and aimed to investigate the potential molecular mechanisms involved. Pretreatment of ex vivo and in vivo I/R-induced rat models by astragaloside IV significantly prevented the ratio of myocardium infarct size, systolic and diastolic dysfunction, and the production of creatine kinase and lactate dehydrogenase. Metabolic analyses showed that I/R injury caused a notable reduction of succinate and elevation of lysophospholipids, indicating excessive reactive oxygen species (ROS) generation driven by succinate’s rapid reoxidization and glycerophospholipid degradation. Molecular validation mechanistically revealed that astragaloside IV stimulated nuclear factor (erythroid-derived 2)-like 2 (Nrf2) released from Kelch-like ECH-associated protein 1 (Keap1) and translocated to the nucleus to combine with musculoaponeurotic fibrosarcoma (Maf) to initiate the transcription of antioxidative gene heme oxygenase-1 (HO-1), which performed a wide range of ROS scavenging processes against pathological oxidative stress in the hearts. As expected, increasing succinate and decreasing lysophospholipid levels were observed in the astragaloside IV-pretreated group compared with the I/R model group. These results suggested that astragaloside IV ameliorated myocardial I/R injury by modulating succinate and lysophospholipid metabolism and scavenging ROS via the Nrf2 signal pathway.
Dissertations / Theses on the topic "Ischemia and reperfusion injury, Creatine/metabolism"
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Almeida, Francine Maria de. "Efeitos da suplementação com creatina na lesão de isquemia e reperfusão após transplante pulmonar unilateral em ratos." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5156/tde-15032018-102313/.
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A lesão de isquemia e reperfusão (IR) é um evento que pode elevar o risco de morte após o transplante pulmonar, por ativar o sistema imune inato a induzir a inflamação. Em situação de isquemia, a oferta de oxigênio se encontra abaixo das necessidades metabólicas, resultando na depleção das reservas celulares de ATP e no aumento da produção de espécies reativas de oxigênio (EROs) e nitrogênio (ERNs). Adicionalmente, a IR desencadeia um processo inflamatório intenso, caracterizado principalmente pela presença de neutrófilos e macrófagos ativados, os quais liberam inúmeros mediadores inflamatórios, perpetuando a inflamação. Nossa hipótese inicial era que a suplementação com creatina (Cr) poderia atenuar a lesão de IR pelo aumento dos níveis de fosfocreatina (PCr) nas células, o que facilitaria a formação de adenosina trifosfato (ATP), promovendo a manutenção dos níveis de Ca2+ intracelular, desestimulando assim a formação de EROs e, consequentemente, diminuindo o processo inflamatório. Portanto, o objetivo do presente estudo foi avaliar o papel da suplementação com creatina na atenuação da lesão de IR em ratos submetidos ao transplante pulmonar, segundo aspectos inflamatórios, estruturais e funcionais do tecido pulmonar. Foram utilizados 64 ratos machos da raça Sprague Dawley distribuídos em quatro grupos: A90, controle/água + 90 minutos de isquemia; Cr90, creatina + 90 minutos de isquemia; A180, controle/água + 180 minutos de isquemia; Cr180, creatina + 180 minutos de isquemia. Os animais doadores receberam creatina (0,5g/kg/dia) diariamente durante cinco dias antes do transplante pulmonar. Os animais do grupo controle receberam apenas o veículo. Após a extração, os pulmões permaneceram em isquemia fria por 90 ou 180 minutos sendo, a seguir, implantados e reperfundidos por 120 minutos. Ao final da reperfusão, foram coletados os dados de mecânica respiratória, além de amostras de ar exalado, sangue arterial e periférico, lavado broncoalveolar e tecido pulmonar. Os parâmetros avaliados foram: resistência das vias aéreas, resistência e elastância do tecido pulmonar, óxido nítrico exalado, pressão parcial de oxigênio e de dióxido de carbono, creatinina sérica, células inflamatórias, índice de edema, PCNA, Caspase-3, TLR 4 e 7, IL1-beta, IL6, TNF-alfa, IL10 e CINC1. Os animais tratados com creatina apresentaram melhora da mecânica pulmonar, dos níveis de creatinina sérica, da gasometria arterial, além da diminuição da fração exalada de óxido nítrico e da inflamação verificada no sangue periférico, no lavado broncoalveolar e no parênquima pulmonar. Estes animais também apresentaram diminuição da proliferação e da apoptose de células inflamatórias, de TLR4, dos níveis de IL6 e CINC1, além de aumento de IL10. Concluímos que o prétratamento com creatina tem efeito protetor na lesão de IR após transplante pulmonar unilateral em ratosIschemia and reperfusion injury (IRI) is an event that can increase the risk of death after lung transplantation (LTx) by activating the innate immune system to induce inflammation. In ischemia events, oxygen supply is below metabolic requirements, resulting in depletion of ATP cellular reserves and increased production of reactive oxygen (ROS) and nitrogen species (RNS). In addition, IRI triggers an intense inflammatory process characterized mainly by the presence of activated neutrophils and macrophages, which release innumerable inflammatory mediators, perpetuating the inflammation. Our initial hypothesis was that creatine supplementation (Cr) could attenuate IRI by increasing phosphocreatine (PCr) levels in cells, which would facilitate the formation of adenosine triphosphate (ATP), promoting the maintenance of intracellular Ca2+ levels, thus discouraging the formation of ROS and, consequently, decreasing the inflammatory process. Therefore, the objective of this study was to evaluate the role of Cr supplementation in the attenuation of IRI in rats underwent to LTx in according to inflammatory, structural and functional aspects of the lung tissue. Sixty Sprague Dawley male rats were distributed into four groups: A90, control / water + 90 minutes of ischemia; Cr90, creatine + 90 minutes of ischemia; A180, control / water + 180 minutes of ischemia; Cr180, creatine + 180 minutes of ischemia. Donor animals received creatine (0.5g/kg/day) daily for five days prior to LTx. Animals in the control group received only the vehicle. The donor`s lung remained in cold ischemia for 90 or 180 minutes and then, were implanted and reperfused during 120 minutes. After reperfusion, respiratory mechanics data were performed and collected samples of exhaled air, arterial and peripheral blood, bronchoalveolar lavage fluid and pulmonary tissue. The parameters evaluated were: airway resistance, resistance and elastance of the pulmonary tissue, exhaled nitric oxide, partial pressure of oxygen and carbon dioxide, serum creatinine, inflammatory cells, edema index, PCNA, Caspase-3, TLR 4 and 7, IL1-beta, IL6, TNF-alpha, IL10, and CINC1. The animals treated with Cr showed an improvement in pulmonary mechanics, serum creatinine levels, and arterial blood gases. In addition, there was a decrease in the exhaled fraction of nitric oxide and in the inflammation in the peripheral blood, BALF, and pulmonary parenchyma in creatine-treated animals. These rats also had a decrease in the proliferation and apoptosis of inflammatory cells, TLR4, IL6, and CINC1. Moreover, there was an increase in the IL10 levels after Cr treatment. We conclude that pre-treatment with Cr has a protective effect on IRI after LTx in rats
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Du, Xiaojian. "Regulation of EphA2 expression in renal ischemia-reperfusion injury." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111599.
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Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury in both native kidneys and renal allografts. Previous studies in our lab have shown that a subset of Eph family receptor tyrosine kinases, including EphA2, is strongly and persistently upregulated in renal tubular cells in both in vitro and in vivo models of the renal IRI. Src kinases are necessary and sufficient for upregulation of EphA2. We have proposed that IRI-induced EphA2 upregulation may serve as a necessary step in renal tubular remodelling.In this study, we have further defined the mechanism of Src kinase-induced EphA2 upregulation by identifying the -145/+137 EphA2 promoter region as the minimal region required for basal and Src kinase-induced activation of the promoter. Moreover, we have identified within this region, at position -45, a canonical cAMP response element (CRE) (Nowakowski et al.), which is essential for EphA2 promoter activation. However, we also found that the prototypical CRE-binding transcription factor, CREB, was not necessary for activation of the EphA2 promoter, suggesting that CREB-related or -unrelated transcription factors are responsible for EphA2 upregulation.
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Westman, Bo. "Studies of ischemia and reperfusion in muscle and liver on glutathione and amino acid metabolism in man /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-406-8/.
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Huo, Jiuzhou. "Regulation of Mitochondrial Calcium Dynamics in Striated Muscle Function." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1595846761184679.
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Maarman, Gerald Jerome. "The effect of CPT-1 inhibition on myocardial function and resistance to ischemia/reperfusion injury in a rodent model of the metabolic syndrome." Thesis, Stellenbosch : University of Stellenbosch, 2010. http://hdl.handle.net/10019.1/5354.
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Thesis (MScMedSc (Dept. of Biomedical Sciences. Medical Physiology))University of Stellenbosch, 2010.ENGLISH ABSTRACT: Background: Obesity is associated with dyslipidemia, insulin resistance and glucose intolerance and together these components characterise the metabolic syndrome (Dandona et al. 2005). In the state of obesity, there are high levels of circulating free fatty acids and increased rates of fatty oxidation which inhibit glucose oxidation. This: (i) reduce the heart‘s contractile ability, (ii) exacerbates ischemic/reperfusion injury and (iii) decreases cardiac mechanical function during reperfusion (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Aim: The aim of our study was to investigate the effect of inhibiting fatty acid oxidation, with oxfenicine (4-Hydroxy-L-phenylglycine), on (i) cardiac mechanical function, (ii) mitochondrial respiration, (iii) myocardial tolerance to ischemia/reperfusion injury, (iv) CPT-I expression, MCAD expression, IRS-1 activation, total GLUT- 4 expression and (v) the RISK pathway (ERK42/44 and PKB/Akt). Methods: Male Wistar rats were fed a control rat chow diet or a high calorie diet (HCD) for 16 weeks. The HCD caused diet induced obesity (DIO). The animals were randomly divided into 4 groups [Control, DIO, Control + oxfen and DIO + oxfen]. The drug was administered for the last 8 weeks of feeding (200mg/kg/day). Animals were sacrificed and the hearts were perfused on the Langendorff perfusion system. After being subjected to regional ischemia and two hours of reperfusion, infarct size was determined. A separate series of animals were fed and/or treated and hearts were collected after 25 minutes global ischemia followed by 30 min reperfusion for determination of GLUT- 4, CPT-1, IRS -1, MCAD, ERK (42/44) and PKB/Akt expression/phosphorylation using Western blot analysis. A third series of hearts were excised and used for the isolation of mitochondria. Results: In the DIO rats, chronic oxfenicine treatment improved cardiac mechanical function by improving mitochondrial respiration. Oxfenicine inhibited CPT-1 expression but had no effect on MCAD or GLUT- 4 expression. Oxfenicine decreased IRS-1 iv expression, but not IRS-1 activation. Oxfenicine also improved myocardial tolerance to ischemia/reperfusion without activation of the RISK pathway (ERK & PKB). In the control rats, chronic oxfenicine treatment worsened cardiac mechanical function by adversely affecting mitochondrial respiration. Oxfenicine also worsened myocardial tolerance to ischemia/reperfusion in the control rats without changes in the RISK pathway (ERK & PKB). Oxfenicine had no effect on CPT-1, MCAD or GLUT- 4 expression. Oxfenicine increased IRS-1 expression, but not IRS-1 activity. Conclusion: Chronic oxfenicine treatment improved cardiac mechanical function and myocardial resistance to ischemia/reperfusion injury in obese animals, but worsened it in control animals. The improved cardiac mechanical function and tolerance to ischemia/reperfusion injury may be due to improvement in mitochondrial respiration.
AFRIKAANSE OPSOMMING: Agtergrond: Vetsug word geassosieer met dislipidemie, insulien weerstandigheid en glukose intoleransie, wat saam die metaboliese sindroom karakteriseer (Dandona et al. 2005). Met vetsug is daar ‗n hoë sirkulasie van vetsure, sowel as verhoogde vertsuur oksidasie wat gevolglik glukose oksidasie onderdruk. Dit: (i) verlaag die hart se vermoë om saam te trek, (ii) vererger isgemiese/herperfusie skade en (iv) verlaag kardiale effektiwiteit gedurende herperfusie (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Doel: Die doel van die studie was om die effekte van vetsuur onderdrukking m.b.v. oksfenisien (4-Hidroksie-L-fenielglisien) op (i) meganiese hart funksie, (ii) mitokondriale respirasie, (iii) miokardiale toleransie teen isgemiese/herperfusie skade, (iv) CPT-I uitdrukking, MCAD uitdrukking, IRS-1 aktiwiteit, totale GLUT-4 uitdrukking en (v) die RISK pad (ERK42/44 en PKB/Akt) te ondersoek. Metodes: Manlike Wistar rotte was gevoer met ‗n kontrole rot dieet of ‗n hoë kalorie dieet (HKD) vir 16 weke. Die HKD lei tot dieet-geïnduseerde vetsug (DGV). Die diere was lukraak verdeel in 4 groepe [kontrole, DGV, kontrole + oksfen en DGV + oksfen]. Die behandeling met die middel was toegedien vir die laaste 8 weke van die voeding protokol (200mg/kg/dag). Die diere was geslag en die harte was geperfuseer op die Langendorff perfusie sisteem. Na blootstelling aan streeks- of globale isgemie en 2 ure herperfusie was infark groottes bepaal. ‗n Aparte reeks diere was gevoer en/of behandel en die harte was versamel na 25 minute globale isgemie gevolg deur 30 minute herperfusie vir die bepaling van GLUT-4, CPT 1, IRS -1, MCAD, ERK (42/44) en PKB/Akt uitdrukking/aktivering d.m.v. Western blot analise. ‗n Derde reeks diere was gebruik vir die isolasie van mitokondria. Resultate: In die DGV diere, het kroniese oksfenisien behandeling meganiese hart funksie verbeter d.m.v. die verbetering van mitokondriale respirasie. Oksfenisien het CPT-1 uitdrukking verlaag terwyl GLUT- 4 en MCAD uitdrukking nie geaffekteer was vi nie. Oksfenisien het IRS-1 uitdrukking verlaag, maar nie IRS-1 aktiwiteit nie. Oksfenisien het ook miokardiale weerstand teen isgemiese/herperfusie verbeter met sonder aktivering van die RISK pad (ERK & PKB). In die kontrole diere, het kroniese oksfenisien behandeling die meganiese hart funksie versleg d.m.v. negatiewe effekte op mitokondriale respirasie. Oksfenisien het die miokardiale weerstand teen isgemiese/herperfusie van die kontrole rotte versleg sonder veranderinge in die RISK pad (ERK & PKB). Oksfenisien het geen effek gehad op CPT-1, MCAD en GLUT-4 uitdrukking nie. Oksfenisien het IRS-1 uitdrukking verhoog, maar nie IRS-1 aktiwiteit nie. Samevatting: Kroniese oksfenisien behandeling het die meganiese hart funksie en miokardiale weerstand teen isgemiese/herperfusie skade in die vet diere verbeter, maar versleg in die kontrole diere. Hierdie verbetering van meganiese hart funksie en weerstand teen isgemiese/herperfusie skade kon dalk wees a.g.v. ‗n verbetering in mitokondriale respirasie.
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Alves, Marcos AntÃnio. "Efeitos da l-alanil-glutamina sobre as concentraÃÃes in vivo de metabÃlitos em ratos submetidos à isquemia-reperfusÃo do membro pÃlvico esquerdo." Universidade Federal do CearÃ, 2005. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=195.
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CoordenaÃÃo de AperfeiÃoamento de NÃvel SuperiorInstituto Dr. Josà Frota
Foram investigados os efeitos metabÃlicos da L-alanil-glutamina nas concentraÃÃes sanguÃneas e teciduais dos metabÃlitos (piruvato, lactato, glicose, acetoacetato, 3-hidroxibutirato, corpos cetÃnicos e ATP) em ratos Wistar submetidos à isquemia/reperfusÃo do membro pÃlvico. Utilizaram-se 96 ratos adultos, machos, distribuÃdos aleatoriamente em 4 grupos numericamente iguais e prÃ-tratados com soluÃÃo salina 2,0 mL (G-1 e G-3) ou L-alanil-glutamina 0,75 g Kg-1(G-2 e G-4), durante 7 dias. Uma hora apÃs a Ãltima gavagem, todos os ratos foram submetidos ao pinÃamento da artÃria ilÃaca esquerda ou operaÃÃo simulada. ApÃs 3 horas a pinÃa foi removida; nos grupos simulados realizou-se nova intervenÃÃo cirÃrgica. Amostras (mÃsculo, fÃgado, rim e sangue) foram coletadas ao final da isquemia mÃxima (T-0) e durante a reperfusÃo (1, 3 e 6h). Os metabÃlitos foram determinados por ensaio enzimÃtico e expressos como MÃdia  E.P.M. Testes nÃo paramÃtricos (Mann-Whitney e Kruskal-Wallis/Dunn) foram utilizados para a anÃlise estatÃstica. O nÃvel de significÃncia foi de p<0,05. NÃo foi evidenciada elevaÃÃo nas concentraÃÃes de lactato, piruvato e glicose durante a lesÃo de isquemia ou reperfusÃo, comparando-se os grupos tratados com soluÃÃo salina (G-1 vs. G-2). Por outro lado houve reduÃÃo nas concentraÃÃes de corpos cetÃnicos em tecido muscular no tempo de isquemia mÃxima e hiperglicemia durante o perÃodo de reperfusÃo. Houve elevaÃÃo nas concentraÃÃes hepÃticas de lactato e glicose muscular e reduÃÃo de lactato no mesmo tecido, nos ratos prÃ-tratados com o dipeptÃdeo. Observou-se ainda, nos mesmos animais, elevaÃÃo das concentraÃÃes de corpos cetÃnicos no fÃgado, no sangue, no mÃsculo e nas concentraÃÃes renais de lactato. Conclui-se, portanto, que o modelo de pinÃamento da artÃria ilÃaca esquerda promove alteraÃÃes metabÃlicas decorrentes da lesÃo de isquemia/reperfusÃo. O dipeptÃdeo L-ALA-GLN induz aumento nas concentraÃÃes hepÃticas de lactato, promove elevaÃÃo de glicose muscular e reduÃÃo de lactato no mesmo tecido indicando aumento no âturn overâ de glicose. O dipeptÃdeo causou aumento da cetogÃnese, cetonemia e captaÃÃo de corpos cetÃnicos durante a reperfusÃo, assim como hiperlactacemia e aumento nas concentraÃÃes renais de lactato. Maior atividade glicolÃtica em tecidos perifÃricos, via ativaÃÃo do ciclo malato-aspartato, levou a diminuiÃÃo da resistÃncia insulÃnica com possÃvel queda de insulinemia, com aumento da cetogÃnese.
A study has been conducted to investigate the effects of L-alanyl-glutamine upon blood and tissue concentrations of metabolites (pyruvate, lactate, glucose, acetoacetato, 3-hydroxybutyrate, ketone bodies and ATP) in Wistar rats subjected to ischemia/reperfusion of hind limb. Ninety-six adult male rats were randomized in 4 groups and pre-treated with saline 2.0 mL (G-1,G-3) or L-alanyl-glutamine solution 0.75 mgKg-1(G-2, G-4) during 7 days. One-hour after the last gavage all rats were submitted to clamping of the left iliac artery or sham operation. The clamp was removed after 3 h; sham rats were operated once more. Muscle, liver, kidney and blood samples were collected at the end of ischemia and at 1-3-6 h during reperfusion. Metabolites were submitted to enzymatic analyses. Results were expressed as Mean  S.E.M. Non-parametric tests (Mann-Whitney and Kruskal-Wallis/Dunn) were utilized for statistical analyses. P<0.05 was accepted as significant. Lactate, pyruvate and glucose concentrations did not increase during ischemia or reperfusion in rats pre-treated with saline (G-1 vs. G-2). On the other hand ketone bodies concentrations were decreased in T-0 and blood glucose was elevated during reperfusion. Liver lactate and muscle glucose were increased and lactate concentration was decreased in L-alanyl-glutamine pre-treated rats. Ketone bodies were elevated in the liver, muscle and blood and renal lactate was also elevated in the aforementioned rats. It is concluded that the model utilized in this study promotes significant metabolic alterations due to ischemia/reperfusion injury. L-Ala-Gln dipeptide induced increased hepatic lactate and muscle glucose concentrations and decreased of muscle lactate concentrations point out to increased turnover of glucose. L-Ala-Gln also induced increased ketogenesis, ketonemia and ketone bodies uptake during reperfusion along with increased lactacidemia and kidney lactate concentrations. Increased glycolytic activity in peripheral tissues via malate-aspartate shuttle activation lead to decreased insulin resistance with possible decrease in plasma insulin levels and increased ketogenesis.
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Wasková, Petra. "Úloha mitochondriální kreatinkinázy a hexokinázy v mechanismech kardioprotektivního působení chronické hypoxie." Doctoral thesis, 2014. http://www.nusl.cz/ntk/nusl-338114.
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IN ENGLISH The ischemia-reperfusion (I/R) injury, which is a consequence of myocardial infarction, represents a major cause of death worldwide. One of the most effective cardioprotective interventions increasing the resistance of hearts to the I/R injury is the adaptation to a chronic hypoxia (CH). However, the molecular mechanisms of CH are still not well understood. The most important factors responsible for the I/R injury are reactive oxygen species (ROS) produced by complexes I and III within the mitochondrial electron transport chain. Potential candidates maintaining ROS at a low level are mitochondrial creatine kinase (mtCK) and two hexokinase isoforms (HK1 and HK2). These enzymes highly support the mitochondrial oxidative phosphorylation by increasing the availability of ADP for complex V of the respiratory chain. In addition, the HK binding to mitochondria inhibits binding of the pro- apoptotic protein BAX, thereby protecting cardiac cells against apoptosis. Besides the mitochondrial CK isoform, there are two cytosolic CK (CKM and CKB) present in cardiomyocytes that help to maintain energy homeostasis. Based on the known anatomical and physiological differences between the left (LV) and the right (RV) ventricles, the first study focused on the comparing ventricles in terms of the energy...
Books on the topic "Ischemia and reperfusion injury, Creatine/metabolism"
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František, Kolář, ed. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.
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Ostadal, Bohuslav. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.
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H, Opie Lionel, ed. Stunning, hibernation, and calcium in myocardial ischemia and reperfusion. Boston: Kluwer Academic, 1992.
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(Editor), Bohuslav Ost'ádal, and Frantisek Kolár (Editor), eds. Cardiac Ischemia: - From Injury to Protection (Basic Science for the Cardiologist). Springer, 1999.
Find full textBook chapters on the topic "Ischemia and reperfusion injury, Creatine/metabolism"
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Bauer, Ph, F. Belleville-Nabet, E. Vauthier, C. Colin, F. Dubois, J. C. Guédenet, O. Bodenreider, et al. "Metabolism of Selenium in a Model of Mesenteric Ischemia-Reperfusion Injury." In Therapeutic Uses of Trace Elements, 229–32. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0167-5_39.
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Elimban, Vijayan, Paramjit S. Tappia, and Naranjan S. Dhalla. "Defects in Mitochondrial Oxidative Phosphorylation in Hearts Subjected to Ischemia-Reperfusion Injury." In Cardiac Energy Metabolism in Health and Disease, 183–97. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1227-8_12.
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Brown, David I., Monte S. Willis, and Jessica M. Berthiaume. "Influence of Ischemia-Reperfusion Injury on Cardiac Metabolism." In The Scientist's Guide to Cardiac Metabolism, 155–67. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-802394-5.00011-x.
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Domaski, Leszek, Karolina Koda, and Kazimierz Ciechanowski. "Ischemia-Reperfusion Injury in the Transplanted Kidney Based on Purine Metabolism Markers and Activity of the Antioxidant System." In Organ Donation and Transplantation - Public Policy and Clinical Perspectives. InTech, 2012. http://dx.doi.org/10.5772/32075.
Full textConference papers on the topic "Ischemia and reperfusion injury, Creatine/metabolism"
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De Almeida, Francine Maria, Angela da Silva Battochio, João Vitor Pithon Napoli, Katiusa Abreu Alves, Manoel Carneiro de Oliveira-Junior, Henrique Takachi Moriya, Paulo Manuel Pêgo-Fernandes, Rodolfo de Paula Vieira, Rogerio Pazetti, and Grace Balbin Silva. "Creatine supplementation attenuates ischemia-reperfusion injury in lung transplantation." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1545.
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