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Luo, Wanjun, Bei Li, Guoqiang Lin, Ri Chen, and Rimao Huang. "Does cardioplegia leave room for postconditioning in paediatric cardiac surgery?" Cardiology in the Young 18, no. 3 (June 2008): 282–87. http://dx.doi.org/10.1017/s1047951108002072.
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AbstractBackgroundPostconditioning by brief episodes of ischaemia performed just at the time of reperfusion have been shown to reduce the size of infarcts in animal models, and in the clinical setting of percutaneous cardiac intervention. The clinical applicability of postconditioning in cardiac surgery remains to be determined. We investigated the effect of postconditioning on myocardial protection in children undergoing cardiac surgery.MethodsWe randomly assigned 40 patients scheduled for surgical correction of congenitally malformed hearts under cold blood cardioplegic arrest to postconditioning or control treatment. Postconditioning was performed by two cycles of 30 seconds ischaemia and 30 seconds reperfusion using aortic reclamping, and declamping started 30 seconds after cardioplegic arrest. We assayed creatine kinase-MB, troponin I, transcardiac release of lactate and neutrophil counts.ResultsThe types of procedure, age, bypass and aortic cross-clamping times were similar in both groups. The postoperative peaks of creatine kinase-MB and troponin I were lower after aortic de-clamping in the postconditioned patients compared with their controls (128 ± 48 units per liter as opposed to 199 ± 79 units per liter, p = 0.016, and 0.34 ± 0.21 nanograms per milliliter as opposed to 0.61 ± 0.53 nanograms per milliliter, p = 0.05), with reduced inotropic scores in those submitted to postconditioning compared with their controls (4.8 ± 3.1 versus 2.3 ± 1.5, p = 0.036). Transcardiac release of lactate was reduced in the postconditioned patients compared with their controls (0.10 ± 0.27 as opposed to 0.37 ± 0.43 millimols per liter, p = 0.048). No differences between groups were found for transcardiac neutrophil count during reperfusion (10.8 ± 6.3% for postconditioning versus 14.0 ± 8.7% for controls, p = 0.48).ConclusionsOur study demonstrates that postconditioning may protect the myocardium of children undergoing cold blood cardioplegic arrest. These data support the need for a larger clinical trial of postconditiong in children undergoing cardiac surgery.
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Vinten-Johansen, Jakob, Derek M. Yellon, and Lionel H. Opie. "Postconditioning." Circulation 112, no. 14 (October 4, 2005): 2085–88. http://dx.doi.org/10.1161/circulationaha.105.569798.
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Heusch, Gerd. "Postconditioning." Journal of the American College of Cardiology 44, no. 5 (September 2004): 1111–12. http://dx.doi.org/10.1016/j.jacc.2004.06.013.
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Couvreur, Nicolas, Laurence Lucats, Renaud Tissier, Alain Bize, Alain Berdeaux, and Bijan Ghaleh. "Differential effects of postconditioning on myocardial stunning and infarction: a study in conscious dogs and anesthetized rabbits." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 3 (September 2006): H1345—H1350. http://dx.doi.org/10.1152/ajpheart.00124.2006.
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Postconditioning, i.e., brief intermittent episodes of myocardial ischemia-reperfusion performed at the onset of reperfusion, reduces infarct size after prolonged ischemia. Our goal was to determine whether postconditioning is protective against myocardial stunning. Accordingly, conscious chronically instrumented dogs (sonomicrometry, coronary balloon occluder) were subjected to a control sequence (10 min coronary artery occlusion, CAO, followed by coronary artery reperfusion, CAR) and a week apart to postconditioning with four cycles of brief CAR and CAO performed at completion of the 10 min CAO. Three postconditioning protocols were investigated, i.e., 15 s CAR/15 s CAO ( n = 5), 30 s CAR/30 s CAO ( n = 7), and 1 min CAR/1 min CAO ( n = 6). Left ventricular wall thickening was abolished during CAO and similarly reduced during subsequent stunning in control and postconditioning sequences (e.g., at 1 h CAR, 33 ± 4 vs. 34 ± 4%, 30 ± 4 vs. 30 ± 4%, and 33 ± 4 vs. 32 ± 4% for 15 s postconditioning, 30 s postconditioning, and 1 min postconditioning vs. corresponding control, respectively). We confirmed this result in anesthetized rabbits by demonstrating that shortening of left ventricular segment length was similarly depressed after 10 min CAO in control and postconditioning sequences (4 cycles of 30 s CAR/30 s CAO). In additional rabbits, the same postconditioning protocol significantly reduced infarct size after 30 min CAO and 3 h CAR (39 ± 7%, n = 6 vs. 56 ± 4%, n = 7 of the area at risk in postconditioning vs. control, respectively). Thus, contrasting to its beneficial effects on myocardial infarction, postconditioning does not protect against myocardial stunning in dogs and rabbits. Conversely, additional episodes of ischemia-reperfusion with postconditioning do not worsen myocardial stunning.
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Sato, Hiroshi, Roberto Bolli, Gregg D. Rokosh, Qiuli Bi, Shujing Dai, Gregg Shirk, and Xian-Liang Tang. "The cardioprotection of the late phase of ischemic preconditioning is enhanced by postconditioning via a COX-2-mediated mechanism in conscious rats." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 4 (October 2007): H2557—H2564. http://dx.doi.org/10.1152/ajpheart.00858.2007.
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The present study sought to determine whether the combination of late preconditioning (PC) with postconditioning enhances the reduction in infarct size. Chronically instrumented rats were assigned to a 45-min ( subset 1) or 60-min ( subset 2) coronary occlusion followed by 24 h of reperfusion. In each subset, rats received no further intervention (control) or were preconditioned 24 h before occlusion (PC), postconditioned at the onset of reperfusion following occlusion, or preconditioned and postconditioned without (PC + postconditioning) or with the COX-2 inhibitor celecoxib (3 mg/kg ip; PC + postconditioning + celecoxib) 10 min before postconditioning. Myocardial cyclooxygenase-2 (COX-2) protein expression and COX-2 activity (assessed as myocardial levels of PGE2) were measured 6 min after reperfusion in an additional five groups (control, PC, postconditioning, PC + postconditioning, and PC + postconditioning + celecoxib) subjected to a 45-min occlusion. PC alone reduced infarct size after a 45-min occlusion but not after a 60-min occlusion. Postconditioning alone did not reduce infarct size in either setting. However, the combination of late PC and postconditioning resulted in a robust infarct-sparing effect in both settings, suggesting additive cardioprotection. Celecoxib completely abrogated the infarct-sparing effect of the combined interventions in both settings. Late PC increased COX-2 protein expression and PGE2 content. PGE2 content (but not COX-2 protein) was further increased by the combination of both interventions, suggesting that postconditioning increases the activity of COX-2 induced by late PC. In conclusion, the combination of late PC and postconditioning produces additive protection, likely due to a postconditioning-induced enhancement of COX-2 activity.
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YAMAKI, IGOR NAGAI, RUY VICTOR SIMÕES PONTES, FELIPE LOBATO DA SILVA COSTA, VITOR NAGAI YAMAKI, RENAN KLEBER COSTA TEIXEIRA, EDSON YUZUR YASOJIMA, and MARCUS VINICIUS HENRIQUES BRITO. "Kidney ischemia and reperfunsion syndrome: effect of lidocaine and local postconditioning." Revista do Colégio Brasileiro de Cirurgiões 43, no. 5 (October 2016): 348–53. http://dx.doi.org/10.1590/0100-69912016005012.
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ABSTRACT Objective: to evaluate the effects of blocking the regulation of vascular tone on the ischemia and reperfusion syndrome in rats through the use of lidocaine in the postconditioning technique. Methods: we randomized 35 rats into seven groups of five animals: Group 1- Control; Group 2- Ischemia and Reperfusion; Group 3- Ischemia, Reperfusion and Saline; Group 4- Ischemic Postconditioning; Group 5- Ischemic Postconditioning and Saline; Group 6- Lidocaine; Group 7- Ischemic Postconditioning and Lidocaine. Except for the control group, all the others were submitted to renal ischemia for 30 minutes. In postconditioning groups, we performed ischemia and reperfusion cycles of five minutes each, applied right after the main ischemia. In saline and lidocaine groups, we instilled the substances at a rate of two drops per minute. To compare the groups, we measured serum levels of urea and creatinine and also held renal histopathology. Results: The postconditioning and postconditioning + lidocaine groups showed a decrease in urea and creatinine values. The lidocaine group showed only a reduction in creatinine values. In histopathology, only the groups submitted to ischemic postconditioning had decreased degree of tubular necrosis. Conclusion: Lidocaine did not block the effects of postconditioning on renal ischemia reperfusion syndrome, and conferred better glomerular protection when applied in conjunction with ischemic postconditioning.
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Kupai, Krisztina, Csaba Csonka, Veronika Fekete, Louise Odendaal, Jacques van Rooyen, De Wet Marais, Tamás Csont, and Péter Ferdinandy. "Cholesterol diet-induced hyperlipidemia impairs the cardioprotective effect of postconditioning: role of peroxynitrite." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 5 (November 2009): H1729—H1735. http://dx.doi.org/10.1152/ajpheart.00484.2009.
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The aim of the present study was to investigate if hyperlipidemia interferes with the infarct size-limiting effect of postconditioning and to study the involvement of peroxynitrite in this phenomenon. Rats were fed a 2% cholesterol-enriched or normal diet for 12 wk. Infarct size by triphenyltetrazolium chloride staining was measured in hearts isolated from both groups and subjected to 30 min coronary occlusion followed by 120 min reperfusion with or without the postconditioning protocol induced by six cycles of 10 s coronary occlusion and 10 s reperfusion at the onset of the reperfusion. Postconditioning significantly decreased infarct size in the normolipidemic but not in the hyperlipidemic group. Postconditioning increased cardiac 3-nitrotyrosine concentration (a marker for peroxynitrite formation) in the normal but not in the cholesterol-fed group when measured at the 5th min of reperfusion. Next, we tested if the postconditioning-induced acute increase in peroxynitrite is involved in the cardioprotection in normolipidemic animals in separate experiments. Postconditioning failed to decrease infarct size in the presence of the peroxynitrite decomposition catalyst 5,10,15,20-tetrakis-[4-sulfonatophenyl]-porphyrinato-iron [III] (20 mg/l) in normolipidemic animals. We conclude that an early increase in peroxynitrite after postconditioning plays a role in cardioprotection. Furthermore, hyperlipidemia blocks the cardioprotective effect of postconditioning at least in part via deterioration of the postconditioning-induced early increase in peroxynitrite formation.
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Pignataro, Giuseppe, Robert Meller, Koichi Inoue, Andrea N. Ordonez, Michelle D. Ashley, Xiong Zhigang, and Roger P. Simon. "In Vivo and In Vitro Characterization of a Novel Neuroprotective Strategy for Stroke: Ischemic Postconditioning." Journal of Cerebral Blood Flow & Metabolism 28, no. 2 (September 19, 2007): 232–41. http://dx.doi.org/10.1038/sj.jcbfm.9600559.
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As clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing, attention has turned to the brain's own endogenous strategies for neuroprotection. Recently, a hypothesis has been offered that modified reperfusion subsequent to a prolonged ischemic episode may also confer ischemic neuroprotection, a phenomenon termed ‘postconditioning’. Here we characterize both in vivo and in vitro models of postconditioning in the brain and offer data suggesting a biological mechanism for protection. Postconditioning treatment reduced infarct volume by up to 50% in vivo and by ∼30% in vitro. A duration of 10 mins of postconditioning ischemia after 10 mins of reperfusion produced the most effective postconditioning condition both in vivo and in vitro. The degree of neuroprotection after postconditioning was equivalent to that observed in models of ischemic preconditioning. However, subjecting the brain to both preconditioning as well as postconditioning did not cause greater protection than each treatment alone. The prosurvival protein kinases extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK), and Akt show prolonged phosphorylation in the cortex of postconditioned rats. Neuroprotection after postconditioning was inhibited only in the presence of LY294002, which blocks Akt activation, but not U0126 or SB203580, which block ERK and P38 MAP kinase activity. In contrast, preconditioning-induced protection was blocked by LY294002, U0126, and SB203580. Our data suggest that postconditioning may represent a novel neuroprotective approach for focal ischemia/reperfusion, and one that is mediated, at least in part, by the activation of the protein kinase Akt.
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Grewal, Amarjot Kaur, Nirmal Singh, and Thakur Gurjeet Singh. "Effects of resveratrol postconditioning on cerebral ischemia in mice: role of the sirtuin-1 pathway." Canadian Journal of Physiology and Pharmacology 97, no. 11 (November 2019): 1094–101. http://dx.doi.org/10.1139/cjpp-2019-0188.
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Evidence has demonstrated that resveratrol preconditioning exhibits neuroprotection against cerebral ischemia–reperfusion (IR) injury. The current investigation aimed to explore whether pharmacological postconditioning, by administering resveratrol, after a sustained ischemia and prior to prolonged reperfusion abrogates cerebral IR injury. Cerebral IR-induced injury mice model was employed in this study to evaluate the neuroprotective effects of pharmacological postconditioning with resveratrol (30 mg/kg; i.p.) administered 5 min before reperfusion. We administered sirtinol, a SIRT1/2 selective inhibitor (10 mg/kg; i.p.) 10 min before ischemia (17 min) and reperfusion (24 h), to elucidate whether the neuroprotection with resveratrol postconditioning depends on SIRT1 activation. Various biochemical and behavioural parameters and histopathological changes were assessed to examine the effect of pharmacological postconditioning. Infarct size is estimated using TTC staining. It was established that resveratrol postconditioning abrogated the deleterious effects of IR injury expressed with regard to biochemical parameters of oxidative stress (TBARS, SOD, GSH), acetylcholinesterase activity, behavioural parameters (memory, motor coordination), infarct size, and histopathological changes. Sirtinol significantly reversed the effect of resveratrol postconditioning. We conclude that induced neuroprotective benefits of resveratrol postconditioning may be the consequence of SIRT1 activation and resveratrol can be considered, for further studies, as potential agent inducing pharmacological postconditioning in clinical situations.
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Pagliaro, Pasquale, and Claudia Penna. "Cardiac Postconditioning." Antioxidants & Redox Signaling 14, no. 5 (March 2011): 777–79. http://dx.doi.org/10.1089/ars.2010.3531.
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Kanazawa, Hideaki, Eleni Tseliou, Konstantinos Malliaras, Kristine Yee, James F. Dawkins, Geoffrey De Couto, Rachel R. Smith, et al. "Cellular Postconditioning." Circulation: Heart Failure 8, no. 2 (March 2015): 322–32. http://dx.doi.org/10.1161/circheartfailure.114.001484.
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Opie, Lionel H., and Sandrine Lecour. "Delayed Postconditioning." Circulation 124, no. 12 (September 20, 2011): 1315–18. http://dx.doi.org/10.1161/circulationaha.111.055400.
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Kerendi, F., H. Kin, M. E. Halkos, R. Jiang, A. J. Zatta, Z. –Q Zhao, R. A. Guyton, and J. Vinten–Johansen. "Remote postconditioning." Basic Research in Cardiology 100, no. 5 (June 17, 2005): 404–12. http://dx.doi.org/10.1007/s00395-005-0539-2.
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Cohen, Michael V., Xi-Ming Yang, and James M. Downey. "The pH Hypothesis of Postconditioning." Circulation 115, no. 14 (April 10, 2007): 1895–903. http://dx.doi.org/10.1161/circulationaha.106.675710.
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Background— It is unclear how reperfusion of infarcting hearts with alternating cycles of coronary reperfusion/occlusion attenuates infarction, but prevention of mitochondrial permeability transition pore (MPTP) formation is crucial. Acidosis also suppresses MPTP formation. We tested whether postconditioning protects by maintaining acidosis during early reoxygenation. Methods and Results— After 30-minute regional ischemia in isolated rabbit hearts, reperfusion with buffer (pH 7.4) caused 34.4±2.2% of the risk zone to infarct, whereas 2 minutes of postconditioning (6 cycles of 10-second reperfusion/10-second occlusion) at reperfusion resulted in 10.7±2.9% infarction. One minute (3 cycles) of postconditioning was not protective. Hypercapnic buffer (pH 6.9) for the first 2 minutes of reperfusion in lieu of postconditioning caused equivalent cardioprotection (15.0±2.6% infarction), whereas 1 minute of acidosis did not protect. Delaying postconditioning (6 cycles) or 2 minutes of acidosis for 1 minute aborted protection. Reperfusion with buffer (pH 7.7) blocked postconditioning protection, but addition of the MPTP closer cyclosporin A restored protection. Reactive oxygen species scavenger N-2-mercaptopropionyl glycine, protein kinase C antagonist chelerythrine, and mitochondrial K ATP channel closer 5-hydroxydecanoate each blocked protection from 2 minutes of acidosis as they did for postconditioning. Conclusion— Thus, postconditioning prevents MPTP formation by maintaining acidosis during the first minutes of reperfusion as reoxygenated myocardium produces reactive oxygen species that activate protective signaling to inhibit MPTP formation after pH normalization.
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Tang, Yan-hua, Jue-shen Yang, Hai-yan Xiang, and Jia-jun Xu. "PI3K-Akt/eNOS in remote postconditioning induced by brief pulmonary ischemia." Clinical & Investigative Medicine 37, no. 1 (February 1, 2014): 26. http://dx.doi.org/10.25011/cim.v37i1.20866.
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Purpose: Postconditioning, a series of brief ischemia-reperfusion sequences given before an ischemic heart undergoes sustained reperfusion, has been shown to lessen ischemia/reperfusion injury. The current study establishes a rabbit model of myocardial ischemia-reperfusion and studied the effects of pulmonary remote postconditioning in this model. Methods: Serum levels of creatine kinase (CK), superoxide dismutase (SOD), and malondialdehyde (MDA), protein expression of endothelial nitric oxide synthase (eNOS), Rho kinase (ROCK- 2), and protein kinase B (Akt) in myocardial cells and the apoptosis index of myocardial cells were examined. Results: Pulmonary remote postconditioning decreased CK, significantly decreased MDA, and increased SOD. Postconditioning significantly increased eNOS protein expression. Administration of eNOS inhibitor, L-NAME, dramatically suppressed the postconditioning-induced eNOS protein expression and serum SOD level, but significantly increased MDA level. The two longer sessions of postconditioning increased Akt, although this increase was not accompanied by changes in levels of the Akt inhibitor, ROCK-2. Blocking eNOS activity with L-NAME had no visible effect on either Akt or ROCK-2. Conclusion: Our results suggest a role for Akt in remote postconditioning-induced myocardial protection, but do not support an involvement of eNOS in Akt-mediated action.
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Jang, Youngho, Jinkun Xi, Huihua Wang, Robert A. Mueller, Edward A. Norfleet, and Zhelong Xu. "Postconditioning Prevents Reperfusion Injury by Activating δ-Opioid Receptors." Anesthesiology 108, no. 2 (February 1, 2008): 243–50. http://dx.doi.org/10.1097/01.anes.0000299437.93898.4a.
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Background While postconditioning has been proposed to protect the heart by targeting the mitochondrial permeability transition pore (mPTP), the detailed mechanism underlying this action is unknown. The authors hypothesized that postconditioning stimulates opioid receptors, which in turn protect the heart from reperfusion injury by targeting the mPTP. Methods Rat hearts (both in vivo and in vitro) were subjected to 30 min of ischemia and 2 h of reperfusion. Postconditioning was elicited by six cycles of 10-s reperfusion and 10-s ischemia. To measure nitric oxide concentration, cardiomyocytes loaded with 4-amino-5-methylamino-2',7'-difluorofluorescein were imaged using confocal microscopy. Mitochondrial membrane potential was determined by loading cardiomyocytes with tetramethylrhodamine ethyl ester. Results In open chest rats, postconditioning reduced infarct size, an effect that was reversed by both naloxone and naltrindole. The antiinfarct effect of postconditioning was also blocked by the mPTP opener atractyloside. In isolated hearts, postconditioning reduced infarct size. Morphine mimicked postconditioning to reduce infarct size, which was abolished by both naltrindole and atractyloside. N-nitro-l-arginine methyl ester and guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one blocked the action of morphine. Further experiments showed that morphine produces nitric oxide in cardiomyocytes by activating delta-opioid receptors. Moreover, morphine could prevent hydrogen peroxide-induced collapse of mitochondrial membrane potential in cardiomyocytes, which was reversed by naltrindole, N-nitro-l-arginine methyl ester, and the protein kinase G inhibitor KT5823. Conclusions Postconditioning protects the heart by targeting the mPTP through activation of delta-opioid receptors. The nitric oxide-cyclic guanosine monophosphate-protein kinase G pathway may account for the effect of postconditioning on the mPTP opening.
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Nepper-Christensen, Lars, Dan Eik Høfsten, Steffen Helqvist, Jens Flensted Lassen, Hans-Henrik Tilsted, Lene Holmvang, Frants Pedersen, et al. "Interaction of ischaemic postconditioning and thrombectomy in patients with ST-elevation myocardial infarction." Heart 106, no. 1 (July 17, 2019): 24–32. http://dx.doi.org/10.1136/heartjnl-2019-314952.
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ObjectiveThe Third Danish Study of Optimal Acute Treatment of Patients with ST-segment Elevation Myocardial Infarction – Ischaemic Postconditioning (DANAMI-3-iPOST) did not show improved clinical outcome in patients with ST-segment elevation myocardial infarction (STEMI) treated with ischaemic postconditioning. However, the use of thrombectomy was frequent and thrombectomy may in itself diminish the effect of ischaemic postconditioning. We evaluated the effect of ischaemic postconditioning in patients included in DANAMI-3-iPOST stratified by the use of thrombectomy.MethodsPatients with STEMI were randomised to conventional primary percutaneous coronary intervention (PCI) or ischaemic postconditioning plus primary PCI. The primary endpoint was a combination of all-cause mortality and hospitalisation for heart failure.ResultsFrom March 2011 until February 2014, 1234 patients were included with a median follow-up period of 35 (interquartile range 28 to 42) months. There was a significant interaction between ischaemic postconditioning and thrombectomy on the primary endpoint (p=0.004). In patients not treated with thrombectomy (n=520), the primary endpoint occurred in 33 patients (10%) who underwent ischaemic postconditioning (n=326) and in 35 patients (18%) who underwent conventional treatment (n=194) (adjusted hazard ratio (HR) 0.55 (95%confidence interval (CI) 0.34 to 0.89), p=0.016). In patients treated with thrombectomy (n=714), there was no significant difference between patients treated with ischaemic postconditioning (n=291) and conventional PCI (n=423) on the primary endpoint (adjusted HR 1.18 (95% CI 0.62 to 2.28), p=0.62).ConclusionsIn this post-hoc study of DANAMI-3-iPOST, ischaemic postconditioning, in addition to primary PCI, was associated with reduced risk of all-cause mortality and hospitalisation for heart failure in patients with STEMI not treated with thrombectomy.Trial registration numberNCT01435408.
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Maslov, Leonid N., S. Yu Tsibul’nikobv, A. V. Tsepokina, M. V. Khutornaya, A. G. Kutikhin, A. V. Gurin, M. V. Basalai, and A. G. Mrochek. "Cardioprotrective effect of remote postconditioning: Mechanisms and possibilities of clinical application." Clinical Medicine (Russian Journal) 94, no. 9 (November 2, 2016): 650–56. http://dx.doi.org/10.18821/0023-2149-2016-94-9-650-656.
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Experimental data indicate that postconditioning at a distance is an effective method for cardiac protection against reperfusion injury. Remote postconditioning prevents reperfusion necrosis and apoptosis of cardiomyocytes, decreases a probability of postinfarction remodeling of the heart. Cardioprotective effect of remote postconditioning depends on the release of tissue factor(s) increasing cardiac tolerance to long-term ischemia-reperfusion after transient ischemia. Clinical investigations show that postconditioning at a distance is an effective method for the prevention of reperfusion injury of the heart during coronary artery bypass surgery.
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Fujita, Masashi, Hiroshi Asanuma, Akio Hirata, Masakatsu Wakeno, Hiroyuki Takahama, Hideyuki Sasaki, Jiyoong Kim, et al. "Prolonged transient acidosis during early reperfusion contributes to the cardioprotective effects of postconditioning." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 4 (April 2007): H2004—H2008. http://dx.doi.org/10.1152/ajpheart.01051.2006.
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We have previously reported that the prolonged transient acidosis during early reperfusion mediates the cardioprotective effects in canine hearts. Recently, postconditioning has been shown to be one of the novel strategies to mediate cardioprotection. We tested the contribution of the prolonged transient acidosis to the cardioprotection of postconditioning. Open-chest anesthetized dogs subjected to 90-min occlusion of the left anterior descending coronary artery and 6-h reperfusion were divided into four groups: 1) control group; no intervention after reperfusion ( n = 6); 2) postconditioning (Postcon) group; four cycles of 1-min reperfusion and 1-min reocclusion ( n = 7); 3) Postcon + sodium bicarbonate (NaHCO3) group; four cycles of 1-min reperfusion and 1-min reocclusion with the administration of NaHCO3( n = 8); and 4) NaHCO3group; administration of NaHCO3without postconditioning ( n = 6). Infarct size, the area at risk (AAR), collateral blood flow during ischemia, and pH in coronary venous blood were measured. The phosphorylation of Akt and extracellular signal-regulated kinase (ERK) in ischemic myocardium was assessed by Western blot analysis. Systemic hemodynamic parameters, AAR, and collateral blood flow were not different among the four groups. Postconditioning induced prolonged transient acidosis during the early reperfusion phase. Administration of NaHCO3completely abolished the infarct size-limiting effects of postconditioning. Furthermore, the phosphorylation of Akt and ERK in ischemic myocardium induced by postconditioning was also blunted by the cotreatment of NaHCO3. In conclusion, postconditioning mediates its cardioprotective effects possibly via prolonged transient acidosis during the early reperfusion phase with the activation of Akt and ERK.
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Jiang, Xiaojing, Chunyu Ai, Enyi Shi, Yoshiki Nakajima, and Hong Ma. "Neuroprotection against Spinal Cord Ischemia–Reperfusion Injury Induced by Different Ischemic Postconditioning Methods." Anesthesiology 111, no. 6 (December 1, 2009): 1197–205. http://dx.doi.org/10.1097/aln.0b013e3181bf1d93.
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Background The authors compared the neuroprotective effects induced by two ischemic postconditioning methods and sought to determine the roles of phosphatidylinositol 3-kinase-Akt and extracellular signal-regulated kinase (ERK) in this neuroprotection. Methods Spinal cord ischemia was induced in rabbits by occlusion of the infrarenal aorta with a balloon catheter for 25 min. Postconditioning was accomplished by either five cycles of 1-min occlusion and 1-min reperfusion (standard postconditioning) or control of the perfusion pressure between 45 and 55 mmHg at the first 10 min of reperfusion (modified postconditioning). Motor function was assessed with the Tarlov score during a 28-day observation period. Histologic examination of lumbar spinal cords was performed. Expressions of Akt and ERK in the spinal cord were evaluated by Western blot. Results Compared with the controls, the two postconditioning methods markedly increased Tarlov scores 1, 3, 7, and 28 days after spinal cord ischemia and number of intact motor neurons in the lumbar spinal cord. No significant difference in Tarlov scores and number of intact motor neurons was detected between the two postconditioning method groups. The two postconditioning methods enhanced the expressions of phospho-Akt and phospho-ERK in spinal cords. The neuroprotective effects and the increases in phospho-Akt and phospho-ERK were abolished by administration of phosphatidylinositol 3-kinase-Akt inhibitor LY-294002 or ERK inhibitor PD-98059. Conclusions The two postconditioning methods possess comparable neuroprotective effects on the spinal cord and share a common molecular mechanism, in which phosphatidylinositol 3-kinase and ERK pathways play crucial roles.
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Dahmani, Souhayl, Danielle Rouelle, Pierre Gressens, and Jean Mantz. "Characterization of the Postconditioning Effect of Dexmedetomidine in Mouse Organotypic Hippocampal Slice Cultures Exposed to Oxygen and Glucose Deprivation." Anesthesiology 112, no. 2 (February 1, 2010): 373–83. http://dx.doi.org/10.1097/aln.0b013e3181ca6982.
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Background There is an increasing interest in the use of dexmedetomidine for anesthesia and sedation. Here, we used the mouse organotypic hippocampal slice culture to investigate whether dexmedetomidine exhibits postconditioning properties against oxygen and glucose deprivation (OGD). The role of the focal adhesion and extracellular-regulated kinases pathways in these effects were examined in both postconditioning and preconditioning. Materials and Methods Slices were obtained from P5 mouse. In postconditioning experiments, Dexmedetomidine (1 microm) was incubated 60 min after the end of OGD. In preconditioning experiments, dexmedetomidine was applied 3 h before OGD. Pharmacologic modulation of the studied pathways was achieved by using selective inhibitors of these cascades. Cell death was assessed 72 h after OGD using propidium iodide labeling and protein expression of activated caspase 3. Results Maximum cell death increased with the duration of OGD. Dexmedetomidine induced a postconditioning effect in the CA1 (but not dentate gyrus) subfield area, which was significantly reduced by modulators of the focal adhesion and the extracellular-regulated kinases pathways. The combination of the inhibitors of the two pathways completely abolished the postconditioning effect of dexmedetomidine. The preconditioning effect of dexmedetomidine against ischemia-induced injury was observed in all hippocampal subfield areas. Results obtained with the pharmacologic modulation used for postconditioning also applied to dexmedetomidine-induced preconditioning. Discussion Dexmedetomidine exhibits significant, but moderate, postconditioning properties against oxygen and glucose deprivation-induced injury. Activation of focal adhesion and the imidazoline 1 receptors-extracellular-regulated kinases pathways is involved in dexmedetomidine-induced postconditioning and preconditioning as well.
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Xie, Ying, Zhengjiang Xing, Jie Wei, Xiaolin Sun, Bin Zhao, Yan Chen, Yue Geng, Zheng Jia, and Honglin Zou. "Levosimendan Postconditioning Attenuates Cardiomyocyte Apoptosis after Myocardial Infarction." Journal of Healthcare Engineering 2022 (January 29, 2022): 1–9. http://dx.doi.org/10.1155/2022/2988756.
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Background. Levosimendan preconditioning has been shown to attenuate myocardial apoptosis in animal models. However, protective effects of levosimendan postconditioning against myocardial apoptosis following myocardial infarction (MI) have not been evaluated. Therefore, we investigated the effects of levosimendan postconditioning on myocardial apoptosis in MI rat models. Methods. In an anoxia/reoxygenation (A/R) model, H9c2 cells were pretreated with or without levosimendan postconditioning after which their apoptosis rates were assessed by flow cytometry, RT-qPCR, and western blot analyses. Then, postconditioning was performed with or without levosimendan in MI rat models. Myocardiocyte apoptosis was evaluated by echocardiography, TTC staining, TUNEL staining, immunohistochemical staining, RT-qPCR, and western blot analysis. Results. Levosimendan postconditioning inhibited H9c2 cell apoptosis in A/R models by elevating Bcl-2 while suppressing Caspase-3 and Bax at both mRNA and protein levels. Moreover, it improved cardiac functions and reduced the left ventricle infarction area in MI rat models. Compared to the MI control group, cardiomyocyte apoptosis rates in the levosimendan postconditioning group were low. The reduced cardiomyocyte apoptosis rates were associated with downregulation of Bax and Caspase-3 as well as with upregulation of Bcl-2 at mRNA and protein levels. Conclusions. Levosimendan postconditioning of MI rat models protected against cardiomyocyte apoptosis, implying that it is a potential strategy for preventing cardiomyocyte apoptosis in the treatment of cardiac dysfunction following MI.
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Fretwell, Laurice, and John M. Dickenson. "Role of large-conductance Ca2+-activated K+ channels in adenosine A1 receptor-mediated pharmacological postconditioning in H9c2 cells." Canadian Journal of Physiology and Pharmacology 89, no. 1 (January 2011): 24–30. http://dx.doi.org/10.1139/y10-106.
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Ischaemic postconditioning is a phenomenon whereby short periods of ischaemia applied during the start of reperfusion protect the myocardium from the damaging consequences of reperfusion. As such, pharmacological-induced postconditioning represents an attractive therapeutic strategy for reducing reperfusion injury during cardiac surgery and following myocardial infarction. The primary aim of this study was to determine the role of large-conductance Ca2+-activated potassium channels (BKCa channels) in adenosine A1 receptor-induced pharmacological postconditioning in the rat embryonic cardiomyoblast-derived cell line H9c2. H9c2 cells were exposed to 6 h hypoxia (0.5% O2) followed by 18 h reoxygenation (H/R) after which cell viability was assessed by monitoring lactate dehydrogenase (LDH) release and caspase-3 activation. The adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA; 100 nmol/L) or the BKCa channel opener NS1619 (10 µmol/L) were added for 30 min at the start of reoxygenation following 6 h hypoxic exposure. Where appropriate, cells were treated (15 min) before pharmacological postconditioning with the BKCa channel blockers paxilline (1 µmol/L) or iberiotoxin (100 nmol/L). Pharmacological postconditioning with CPA or NS1619 significantly reduced H/R-induced LDH release. Treatment with paxilline or iberiotoxin attenuated adenosine A1 receptor and NS1619-induced pharmacological postconditioning. These results have shown for the first time that BKCa channels are involved in adenosine A1 receptor-induced pharmacological postconditioning in a cell model system.
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Ozkisacik, Sezen, Ali Onur Erdem, Barlas Etensel, Canten Tataroglu, Mukadder Serter, and Mesut Yazici. "Short-interval postconditioning protects the bowel against ischaemia–reperfusion injury in rats." Journal of International Medical Research 45, no. 3 (May 28, 2017): 1036–41. http://dx.doi.org/10.1177/0300060517708921.
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Objective Acute mesenteric ischaemia leads to intestinal damage. Restoration of blood flow results in further damage to tissue, which is called reperfusion injury. This study aimed to investigate the protective effects of short-interval postconditioning and to determine the optimal interval for reperfusion in an experimental rat model of intestinal ischaemia. Methods Forty adult male Wistar rats were grouped as follows: sham (Sh), ischaemia + reperfusion (IR), ischaemia + postconditioning for 5 seconds (PC5), ischaemia + postconditioning for 10 seconds (PC10), and ischaemia + postconditioning for 20 seconds (PC20). For postconditioning, 10 cycles of reperfusion (5, 10, or 20 seconds) interspersed by 10 cycles of 10 seconds of ischaemia were performed. Blood glutathione reductase (GR) and glutathione peroxidase (GPx) levels were measured. Intestinal tissue damage was assessed histopathologically. Results GR levels were significantly higher in the PC5 group than in the IR group (37.7 ± 9.0 vs. 18.5 ± 2.0 min/g Hb). GPx levels were significantly higher in the PC10 group than in the IR group (43.2 ± 9.2 vs. 15.9 ± 4.6 U/g Hb). The histopathological score was significantly lower in the PC5 group (1.1 ± 0.1) than in the IR group (2.1 ± 0.2). Conclusion Short-interval postconditioning reduces reperfusion injury in the ischaemic bowel and the optimal interval for reperfusion is 5 seconds. The long-term effects of short-interval postconditioning and the optimal reperfusion interval in intestinal ischaemia–reperfusion in rats need to be investigated.
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Tang, Y., A. Mennander, N. Oksala, M. Atalay, H. Syvala, A. Lagerstedt, M. Kuuslahti, et al. "Postconditioning and Remote Postconditioning of Ischemic Rat Cardiac Grafts." European Surgical Research 45, no. 1 (2010): 1–8. http://dx.doi.org/10.1159/000315479.
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Zhao, Heng. "Ischemic Postconditioning as a Novel Avenue to Protect against Brain Injury after Stroke." Journal of Cerebral Blood Flow & Metabolism 29, no. 5 (February 25, 2009): 873–85. http://dx.doi.org/10.1038/jcbfm.2009.13.
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Ischemic postconditioning initially referred to a stuttering reperfusion performed immediately after reperfusion, for preventing ischemia/reperfusion injury in both myocardial and cerebral infarction. It has evolved into a concept that can be induced by a broad range of stimuli or triggers, and may even be performed as late as 6 h after focal ischemia and 2 days after transient global ischemia. The concept is thought to be derived from ischemic preconditioning or partial/gradual reperfusion, but in fact the first experiment for postconditioning was carried out much earlier than that of preconditioning or partial/gradual reperfusion, in the research on myocardial ischemia. This review first examines the protective effects and parameters of postconditioning in various cerebral ischemic models. Thereafter, it provides insights into the protective mechanisms of postconditioning associated with reperfusion injury and the Akt, mitogen-activated protein kinase (MAPK), protein kinase C (PKC), and ATP-sensitive K+ (KATP) channel cell signaling pathways. Finally, some open issues and future challenges regarding clinical translation of postconditioning are discussed.
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Шурыгин, Mikhail Shurygin, Шурыгина, Irina Shurygina, Дремина, and Natalya Dremina. "POSTCONDITIONING AS A METHOD TISSUE SURVIVABILITY ENHANCEMENT IN ISCHEMIC DAMAGE." Бюллетень Восточно-Сибирского научного центра Сибирского отделения Российской академии медицинских наук 1, no. 4 (November 28, 2016): 183–86. http://dx.doi.org/10.12737/23030.
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The article presents the present-day data on the phenomenon of ischemic myocardial postconditioning. It has been shown, that this phenomenon consists in protection of the heart from reperfusion damage by the means of short episodes of ischemia/reperfusion performed at the early stage after prolonged ischemia. It is presented that postconditioning effect manifests in limiting the size of infarction and preserving endothelial function in the region exposed to ischemic injury. The article reports on the modern concept of role of various intracellular signal cascades in providing survival of the cell after the episode of ischemia/reperfusion. Much attention is given to changing in the state of pores localized in internal mitochondrial membrane as end links of realization of postconditioning effect. Prospects of clinical use of postconditioning are very optimistic due to the fact that application of different variants of preconditioning is limited because in most cases it is impossible to predict the time of occurrence of ischemic injury, whereas postconditioning may be used after prolonged ischemia.
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Sapmaz, Ali, A. Tulga Ulus, Nilüfer N. Turan, F. Figen Kaymaz, Hija Yazıcıoğlu, Siyar Ersöz, Erdal Simsek, and Cüneyt Köksoy. "Which type of conditioning method protects the spinal cord from the ischemia–reperfusion injury in 24 hours?" Vascular 23, no. 6 (February 2, 2015): 614–21. http://dx.doi.org/10.1177/1708538114568702.
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Objective This study was designed to test the effects of different types of preconditioning and postconditioning methods on spinal cord protection following aortic clamping. Methods The animals (rabbits) were divided into sham-operated, ischemic preconditioning, remote ischemic preconditioning, simultaneous aortic and ischemic remote preconditioning, and ischemic postconditioning groups. After neurological evaluations, ultrastructural analysis and immunohistochemical staining for caspase-3 were evaluated after 24 h following ischemia. Results The neurological outcomes of the remote ischemic preconditioning (4.2 ± 0.4) and ischemic postconditioning (4.6 ± 0.8) groups were significantly improved when compared with the ischemia group (2.2 ± 04). The immunohistochemical analysis revealed that the lowest percentage of apoptosis was in-group ischemic preconditioning at 12.5 ± 30.6%. In the comparison of intracellular edema in an ultrastructural analysis, the ischemic preconditioning and ischemic postconditioning groups had significantly lower values than the ischemia group. Conclusion The conditioning methods attenuate ischemia–reperfusion injury for spinal cord injury. Ischemic and remote preconditioning and also postconditioning methods are simple to perform and inexpensive.
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Ma, Di, Liangshu Feng, Fang Deng, and Jia-Chun Feng. "Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning." BioMed Research International 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/6891645.
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Research on attenuating the structural and functional deficits observed following ischemia-reperfusion has become increasingly focused on the therapeutic potential of ischemic postconditioning. In recent years, various methods and animal models of ischemic postconditioning have been utilized. The results of these numerous studies have indicated that the mechanisms underlying the neuroprotective effects of ischemic postconditioning may involve reductions in the generation of free radicals and inhibition of calcium overload, as well as the release of endogenous active substances, alterations in membrane channel function, and activation of protein kinases. Here we review the novel discovery, mechanism, key factors, and clinical application of ischemic postconditioning and discuss its implications for future research and problem of clinical practice.
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Dragoni, Saverio, Giuseppe Di Stolfo, Silvia Sicuro, Monica Lisi, John D. Parker, Sandro Forconi, and Tommaso Gori. "Postconditioning fails to prevent radial artery endothelial dysfunction induced by ischemia and reperfusion: evidence from a human in vivo study." Canadian Journal of Physiology and Pharmacology 84, no. 6 (June 2006): 611–15. http://dx.doi.org/10.1139/y05-160.
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Animal studies have shown that, as compared with unrestricted reperfusion, exposure to brief periods of controlled ischemia (postconditioning) at the end of a prolonged ischemia reduces the extent of tissue damage. We set out to test whether postconditioning can prevent endothelial dysfunction induced by ischemia and reperfusion in a human in vivo model. Ten healthy young non-smoking volunteers were enrolled in this cross-over, controlled, investigator-blinded study. Subjects were exposed to 15 min of forearm ischemia followed by either unrestricted reperfusion or postconditioning (3 periods of 20 s of ischemia separated by 10 s of reperfusion). Endothelium-dependent flow-mediated dilation (FMD) was measured at the level of the radial artery before and after ischemia (with or without postconditioning). Forearm ischemia blunted FMD in both study visits (unrestricted reperfusion visit: before ischemia, 7.7% ± 1.3%; after ischemia, 2.5% ± 1.4%; and postconditioning visit: before, 7.3% ± 1.2%; after, 2.6 ± 1.6%; P < 0.05 for both, P = not significant (NS) between visits). In contrast with data from animal studies, postconditioning (20 s ischemia – 10 s reperfusion repeated 3 times) does not limit post-ischemic endothelial dysfunction in this human in vivo model. Further human studies are necessary to evaluate other reperfusion protocols in an attempt to limit post-ischemic tissue damage.
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Li, Zy, B. Liu, J. Yu, Fw Yang, Yn Luo, and Pf Ge. "Ischaemic Postconditioning Rescues Brain Injury Caused by Focal Ischaemia/Reperfusion via Attenuation of Protein Oxidization." Journal of International Medical Research 40, no. 3 (June 2012): 954–66. http://dx.doi.org/10.1177/147323001204000314.
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OBJECTIVE: To investigate the effects of ischaemic postconditioning on brain injury and protein oxidization in focal ischaemia/reperfusion. METHODS: Adult male Wistar rats ( n = 30) were randomly divided into sham-operated, ischaemia, and ischaemic postconditioning groups. Ischaemia was produced by middle cerebral artery occlusion and ischaemic postconditioning was performed using three cycles of 30-s/30-s reperfusion/reocclusion after 2 h of ischaemia. Brain infarction size, hydrogen peroxide concentration, superoxide dismutase (SOD), catalase (CAT) and proteasome activities, protein carbonyl derivatives and advanced oxidized protein products (AOPPs) were evaluated. RESULTS: The size of brain infarction after ischaemic postconditioning was significantly smaller compared with the ischaemia group, and was concomitant with significant reduction in protein carbonyl derivatives and AOPPs. The activities of SOD, CAT and proteasomes were elevated by ischaemic postconditioning compared with the ischaemia group. CONCLUSIONS: Ischaemic post-conditioning is an effective way of reducing the size and effects of brain infarction caused by focal ischaemia/reperfusion, possibly due to a decrease in oxidized protein levels. Decreasing protein oxidization may, therefore, be a useful target for preventing cerebral injury.
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Pignataro, Giuseppe, Elga Esposito, Ornella Cuomo, Rossana Sirabella, Francesca Boscia, Natascia Guida, Gianfranco Di Renzo, and Lucio Annunziato. "The NCX3 Isoform of the Na+/Ca2+ Exchanger Contributes to Neuroprotection Elicited by Ischemic Postconditioning." Journal of Cerebral Blood Flow & Metabolism 31, no. 1 (July 14, 2010): 362–70. http://dx.doi.org/10.1038/jcbfm.2010.100.
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It has been recently shown that a short sublethal brain ischemia subsequent to a prolonged harmful ischemic episode may confer ischemic neuroprotection, a phenomenon termed ischemic postconditioning. Na+/Ca2+ exchanger (NCX) isoforms, NCX1, NCX2, and NCX3, are plasma membrane ionic transporters widely distributed in the brain and involved in the control of Na+ and Ca2+ homeostasis and in the progression of stroke damage. The objective of this study was to evaluate the role of these three proteins in the postconditioning-induced neuroprotection. The NCX protein and mRNA expression was evaluated at different time points in the ischemic temporoparietal cortex of rats subjected to tMCAO alone or to tMCAO plus ischemic postconditioning. The results of this study showed that NCX3 protein and ncx3 mRNA were upregulated in those brain regions protected by postconditioning treatment. These changes in NCX3 expression were mediated by the phosphorylated form of the ubiquitously expressed serine/threonine protein kinase p-AKT, as the p-AKT inhibition prevented NCX3 upregulation. The relevant role of NCX3 during postconditioning was further confirmed by results showing that NCX3 silencing, induced by intracerebroventricular infusion of small interfering RNA (siRNA), partially reverted the postconditioning-induced neuroprotection. The results of this study support the idea that the enhancement of NCX3 expression and activity might represent a reasonable strategy to reduce the infarct extension after stroke.
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Raphael, Jacob, Yaacov Gozal, Nachum Navot, and Zhiyi Zuo. "Activation of Adenosine Triphosphate–regulated Potassium Channels during Reperfusion Restores Isoflurane Postconditioning-induced Cardiac Protection in Acutely Hyperglycemic Rabbits." Anesthesiology 122, no. 6 (June 1, 2015): 1299–311. http://dx.doi.org/10.1097/aln.0000000000000648.
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Abstract Background: Hyperglycemia is known to inhibit myocardial anesthetic postconditioning. The authors tested whether activation of adenosine triphosphate–regulated potassium (KATP) channels would restore anesthetic postconditioning during acute hyperglycemia. Methods: Rabbits subjected to 40-min myocardial ischemia and 3-h reperfusion (ischemia–reperfusion [I/R]) were assigned to groups (n = 10 in each group) with or without isoflurane postconditioning (2.1% for 5 min) in the presence or absence of hyperglycemia and/or the KATP channel agonist diazoxide. Creatine kinase MB fraction and infarct size were measured. Phosphorylated protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS) were assessed. Oxidative stress was evaluated by measuring malondialdehyde, and apoptosis was assessed by dUTP nick-end labeling and activated caspase-3. Results: Postconditioning significantly reduced myocardial infarct size (26 ± 4% in the isoflurane [ISO] group vs. 53 ± 2% in the I/R group; P = 0.007); whereas, hyperglycemia inhibited this effect (infarct size: 47 ± 2%, P = 0.02 vs. the ISO group). Phosphorylated and eNOS levels increased, whereas malondialdehyde and myocardial apoptosis were significantly lower after isoflurane postconditioning compared with I/R. These effects were inhibited by acute hyperglycemia. Diazoxide restored the protective effect of isoflurane in the hyperglycemic animals (infarct size: 29 ± 2%; P = 0.01 vs. the I/R group), reduced malondialdehyde levels and myocardial apoptosis, but did not affect the expression of phosphorylated Akt or eNOS. Conclusions: KATP channel activation restored anesthetic postconditioning-induced myocardial protection under acute hyperglycemia. This effect occurred without increasing Akt or eNOS phosphorylation, suggesting that KATP channels are located downstream to Akt and eNOS in the pathway of isoflurane-induced myocardial postconditioning.
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Zhang, Xuan, Qiang Fu, Longhe Xu, Yitian Yang, Weixing Zhao, Yunliang Zhang, Hao Li, and Weidong Mi. "Dexmedetomidine Postconditioning Alleviates Hypoxia/Reoxygenation Injury in Senescent Myocardial Cells by Regulating lncRNA H19 and m6A Modification." Oxidative Medicine and Cellular Longevity 2020 (January 7, 2020): 1–13. http://dx.doi.org/10.1155/2020/9250512.
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H19, a long noncoding RNA (lncRNA), reportedly protects myocardial cells (H9c2 cell line) against hypoxia-reoxygenation- (H/R-) induced injury. Dexmedetomidine (Dex) has an important myocardial protective effect, although its function and mechanism in cardiac ischemia/reperfusion (I/R) injury, especially for senile patients, requires further study. RNA N6-methyladenosine (m6A) is the most abundant endogenous RNA modification. However, the effect of Dex postconditioning on RNA m6A modification has rarely been reported. The aim of this study was to evaluate roles of H19 and m6A modification in Dex postconditioning of aged cardiomyocytes. Hydrogen peroxide (H2O2) was used to induce senescence of H9c2 cells. After 6 h of hypoxia, H9c2 cells were exposed to different concentrations of dexmedetomidine (0, 500 nM, 1 μM, and 2 μM) for 6 h. After knockdown or overexpression of H19 and its downstream gene miR-29b-3p and cellular inhibitor of apoptosis protein 1 (cIAP1), Dex postconditioning experiments were performed to examine effects on myocardial cell injury. Global m6A levels after H/R with or without Dex postconditioning were measured with a colorimetric m6A RNA Methylation Quantification Kit. The mechanism by which RNA m6A methylation regulated genes mediating H19 expression was verified by m6A RNA immunoprecipitation (MeRIP), and the function of Dex postconditioning of aged cardiomyocytes was investigated. Dex postconditioning protected against H/R-induced injury of aged myocardial cells through H19/miR-29b-3p/cIAP1, increased methylation of RNA m6A elicited by H/R, and attenuated H/R-induced injury by suppressing expression of the RNA m6A demethylase gene alkB homolog 5 (ALKBH5). In addition, AKLBH5 regulated the expression of H19, and Dex postconditioning attenuated H/R-induced injury via ALKBH5 in aged cardiomyocytes.
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Boengler, Kerstin, Gerd Heusch, and Rainer Schulz. "Mitochondria in Postconditioning." Antioxidants & Redox Signaling 14, no. 5 (March 2011): 863–80. http://dx.doi.org/10.1089/ars.2010.3309.
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Thibault, Hélène, Christophe Piot, and Michel Ovize. "Postconditioning in man." Heart Failure Reviews 12, no. 3-4 (May 24, 2007): 245–48. http://dx.doi.org/10.1007/s10741-007-9033-2.
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Liu, Wei, Liping Huang, Xue Liu, Li Zhu, Yan Gu, Wei Tian, Lin Zhang, Shengli Deng, and Tian Yu. "Urocortin I Protects against Myocardial Ischemia/Reperfusion Injury by Sustaining Respiratory Function and Cardiolipin Content via Mitochondrial ATP-Sensitive Potassium Channel Opening." Oxidative Medicine and Cellular Longevity 2022 (March 29, 2022): 1–20. http://dx.doi.org/10.1155/2022/7929784.
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Objective. Our experiments were aimed at probing whether urocortin I postconditioning was beneficial for maintaining the mitochondrial respiratory function and inhibiting the surging of reactive oxygen species. In addition, our experiments also intended to reveal the relationships between urocortin I postconditioning and mitochondrial ATP-sensitive potassium channel. Methods. Langendorff and MPA perfusion systems were used to establish myocardial ischemia-reperfusion injury model and cardiomyocytes hypoxia-reoxygenation injury model in rats, respectively. Isolated hearts and cardiomyocytes were randomly divided into normal group, ischemia-reperfusion/hypoxia-reoxygenation group, urocortin I postconditioning group, and 5-hydroxysolanoic acid (5-HD)+urocortin I group. At the end of balance (T1) and reperfusion (T2), cardiac functions, mitochondrial state3 respiratory, respiratory control ratio, mitochondrial respiratory enzyme activity, and mitochondrial cardiolipin content were measured. Our experiments also observed the ultrastructure of myocardium. The changes of cardiomyocyte mitochondrial permeability transition pore, mitochondrial membrane potential, reactive oxygen species, expression of apoptosis protein, and cardiomyocytes activity were detected at the end of reoxygenation. Results. The cardiac functions, mitochondrial respiratory function, and enzyme activity of the normal group were better than other three groups at T2, and urocortin I postconditioning group was better than the IR group and 5-HD+urocortin I group. LVEDP, +dp/dtmax, mitochondrial respiratory function, and enzyme activity of IR group were worse than 5-HD+urocortin I group. Cardiolipin content of the normal group was higher than the other three groups at T2, urocortin I postconditioning group was higher than the IR group and 5-HD+urocortin I group, and 5-HD+urocortin I group was still higher than the IR group. The ultrastructure of the normal group maintained the most integrated than the other groups, IR group suffered the most serious damage, and ultrastructure of the urocortin I postconditioning group was better than the IR group and 5-HD+urocortin I group. At the end of reoxygenation, activity of mitochondrial permeability transition pore and generation of reactive oxygen species of normal group were lower than the other groups, HR group and 5-HD+urocortin I group were higher than the urocortin I postconditioning group, and 5-HD+urocortin I group was still higher than the urocortin I postconditioning group. Normal group had the highest level of mitochondrial membrane potential at the end of reoxygenation, and the urocortin I postconditioning group was higher than the HR group and 5-HD+urocortin I group. The normal group had the lowest expression level of Bax and the highest expression level of Bcl-2 at the end of reoxygenation. Urocortin I postconditioning group had lower Bax expression but higher Bcl-2 expression than the HR and 5-HD+urocortin I group. Accordingly, the normal group had the highest activity of cardiomyocytes, and the urocortin I postconditioning group was higher than the HR group and 5-HD+urocortin I group. Conclusions. Urocortin I postconditioning can protect the activity of cardiomyocytes after hypoxia-reoxygenation injury, improve the mitochondrial respiratory function, and enhance the contractility of isolated heart after myocardial ischemia-reperfusion injury. The alleviation of myocardial injury relates to the opening of mitochondrial ATP-sensitive potassium channel.
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Yang, Mu, Jian-Xin Dong, Lu-Bin Li, Hai-Jie Che, Jun Yong, Fu-Bo Song, Tao Wang, and Jv-Wen Zhang. "Local and Remote Postconditioning Decrease Intestinal Injury in a Rabbit Ischemia/Reperfusion Model." Gastroenterology Research and Practice 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/2604032.
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Intestinal ischemia/reperfusion (I/R) injury is a significant problem that is associated with high morbidity and mortality in critical settings. This injury may be ameliorated using postconditioning protocol. In our study, we created a rabbit intestinal I/R injury model to analyze the effects of local ischemia postconditioning (LIPo) and remote ischemia postconditioning (RIPo) on intestinal I/R injury. We concluded that LIPo affords protection in intestinal I/R injury in a comparable fashion with RIPo by decreasing oxidative stress, neutrophil activation, and apoptosis.
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Chiari, Pascal C., Martin W. Bienengraeber, Paul S. Pagel, John G. Krolikowski, Judy R. Kersten, and David C. Warltier. "Isoflurane Protects against Myocardial Infarction during Early Reperfusion by Activation of Phosphatidylinositol-3-Kinase Signal Transduction: Evidence for Anesthetic-induced Postconditioning in Rabbits." Anesthesiology 102, no. 1 (January 1, 2005): 102–9. http://dx.doi.org/10.1097/00000542-200501000-00018.
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Background Brief episodes of ischemia during early reperfusion after coronary occlusion reduce the extent of myocardial infarction. Phosphatidylinositol-3-kinase (PI3K) signaling has been implicated in this "postconditioning" phenomenon. The authors tested the hypothesis that isoflurane produces cardioprotection during early reperfusion after myocardial ischemia by a PI3K-dependent mechanism. Methods Pentobarbital-anesthetized rabbits (n = 80) subjected to a 30-min coronary occlusion followed by 3 h reperfusion were assigned to receive saline (control), three cycles of postconditioning ischemia (10 or 20 s each), isoflurane (0.5 or 1.0 minimum alveolar concentration), or the PI3K inhibitor wortmannin (0.6 mg/kg, intravenously) or its vehicle dimethyl sulfoxide. Additional groups of rabbits were exposed to combined postconditioning ischemia (10 s) and 0.5 minimum alveolar concentration isoflurane in the presence and absence of wortmannin. Phosphorylation of Akt, a downstream target of PI3K, was assessed by Western blotting. Results Postconditioning ischemia for 20 s, but not 10 s, reduced infarct size (P < 0.05) (triphenyltetrazolium staining; 20 +/- 3% and 34 +/- 3% of the left ventricular area at risk, respectively) as compared with control (41 +/- 2%). Exposure to 1.0, but not 0.5, minimum alveolar concentration isoflurane decreased infarct size (21 +/- 2% and 43 +/- 3%, respectively). Wortmannin abolished the protective effects of postconditioning (20 s) and 1.0 minimum alveolar concentration isoflurane. Combined postconditioning (10 s) and 0.5 minimum alveolar concentration isoflurane markedly reduced infarct size (17 +/- 5%). This action was also abolished by wortmannin (44 +/- 2%). Isoflurane (1.0 minimum alveolar concentration) increased Akt phosphorylation after ischemia (32 +/- 6%), and this action was blocked by wortmannin. Conclusions Isoflurane acts during early reperfusion after prolonged ischemia to salvage myocardium from infarction and reduces the threshold of ischemic postconditioning by activating PI3K.
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Zatta, Amanda J., Hajime Kin, Darice Yoshishige, Rong Jiang, Ningping Wang, James G. Reeves, James Mykytenko, et al. "Evidence that cardioprotection by postconditioning involves preservation of myocardial opioid content and selective opioid receptor activation." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 3 (March 2008): H1444—H1451. http://dx.doi.org/10.1152/ajpheart.01279.2006.
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Opioids introduced at reperfusion (R) following ischemia (I) reduce infarct size much like postconditioning, suggesting the hypothesis that postconditioning increases cardiac opioids and activates local opioid receptors. Anesthetized male rats subjected to 30 min regional I and 3 h R were postconditioned with three cycles of 10 s R and 10 s reocclusion at onset of R. Naloxone (NL), its peripherally restricted analog naloxone methiodide, δ-opioid receptor (DOR) antagonist naltrindole (NTI), κ-opioid receptor antagonist norbinaltorphimine (NorBNI), and μ-opioid receptor (MOR) antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) were administered intravenously 5 min before R. The area at risk (AAR) was comparable among groups, and postconditioning reduced infarct size from 57 ± 2 to 42 ± 2% ( P < 0.05). None of the antagonists alone altered infarct size. All antagonists abrogated postconditioning protection at higher doses. However, blockade of infarct sparing by postconditioning was lost, since tested doses of NL, NTI, NorBNI, and CTAP were lowered. The efficacy of NorBNI declined first at 3.4 μmol/kg, followed sequentially by NTI (1.1), NL (0.37), and CTAP (0.09), suggesting likely MOR and perhaps DOR participation. Representative small, intermediate, and large enkephalins in the AAR were quantified (fmol/mg protein; mean ± SE). I/R reduced proenkephalin (58 ± 9 vs. 33 ± 4; P < 0.05) and sum total of measured enkephalins, including proenkephalin, peptide B, methionine-enkephalin, and methionine-enkephalin-arginine-phenylalanine (139 ± 17 vs. 104 ± 7; P < 0.05) compared with shams. Postconditioning increased total enkephalins (89 ± 8 vs. 135 ± 5; P < 0.05) largely by increasing proenkephalin (33 ± 4 vs. 96 ± 7; P < 0.05). Thus the infarct-sparing effect of postconditioning appeared to involve endogenously activated MORs and possibly DORs, and preservation of enkephalin precursor synthesis in the AAR.
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Ertugrul, Imran A., Vincent van Suylen, Kevin Damman, Marie-Sophie L. Y. de Koning, Harry van Goor, and Michiel E. Erasmus. "Donor Heart Preservation with Hydrogen Sulfide: A Systematic Review and Meta-Analysis." International Journal of Molecular Sciences 22, no. 11 (May 27, 2021): 5737. http://dx.doi.org/10.3390/ijms22115737.
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Preclinical studies have shown that postconditioning with hydrogen sulfide (H2S) exerts cardioprotective effects against myocardial ischemia-reperfusion injury (IRI). The aim of this study was to appraise the current evidence of the cardioprotective effects of H2S against IRI in order to explore the future implementation of H2S in clinical cardiac transplantation. The current literature on H2S postconditioning in the setting of global myocardial ischemia was systematically reviewed and analyzed, performing meta-analyses. A literature search of the electronic databases Medline, Embase and Cinahl identified 1835 studies that were subjected to our pre-defined inclusion criteria. Sixteen studies were considered eligible for inclusion. Postconditioning with H2S showed significant robust effects with regard to limiting infarct size (standardized mean difference (SMD) = −4.12, 95% CI [−5.53–−2.71], p < 0.00001). Furthermore, H2S postconditioning consistently resulted in a significantly lower release of cardiac injury markers, lower levels of oxidative stress and improved cardiac function. Postconditioning with slow-releasing H2S donors offers a valuable opportunity for novel therapies within cardiac preservation for transplantation. Before clinical implication, studies evaluating the long-term effects of H2S treatment and effects of H2S treatment in large animal studies are warranted.
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Teixeira, Antonio Roberto Franchi, Nilza T. Molan, Márcia Saldanha Kubrusly, Marta Bellodi-Privato, Ana Maria Coelho, Kátia R. Leite, Marcel Autran Cesar Machado, Telésforo Bacchella, and Marcel Cerqueira César Machado. "Postconditioning ameliorates lipid peroxidation in liver ischemia-reperfusion injury in rats." Acta Cirurgica Brasileira 24, no. 1 (February 2009): 52–56. http://dx.doi.org/10.1590/s0102-86502009000100011.
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PURPOSE: Liver ischemia-reperfusion injury is a phenomenon presents in events like liver resections and transplantation. The restoration of blood flow may leads to local and systemic injury. Several techniques have been developed in order to avoid or ameliorate ischemia-reperfusion injury in clinical situations. The application of a sttuter reperfusion after the ischemic event (postconditioning) could alters the hydrodynamics and stimulates endogenous mechanisms that attenuate the reperfusion injury. The present study was designed to evaluate the potential protective effect of postconditioning in a model of ischemia-reperfusion in rats. METHODS: Hepatic anterior pedicle of median and left anterolateral segments were exposed and clamped for 1 hour. Two hours later, clamp was released in two different ways: Control Group (n=7): clamp was release straightforward; Postconditioning Group (n=7): clamp was released intermittently. Lipid peroxidation (malondialdehyde) and expression of the glutathione-s-transferase-α-3 gene were studied. RESULTS: Lipid peroxidation was significantly decreased in ischemic and non-ischemic liver by postconditioning. GST- α3 gene was overexpressed in postconditioned group, but not significantly. CONCLUSION: Postconditioning induced hepatoprotection by reducing lipid peroxidation in the ischemic and non-ischemic liver.
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Duerr, Georg Daniel, Shuijing Wu, Max Lukas Schneider, Vanessa Marggraf, Christina Katharina Weisheit, Markus Velten, Luise Verfuerth, et al. "CpG postconditioning after reperfused myocardial infarction is associated with modulated inflammation, less apoptosis, and better left ventricular function." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 5 (November 1, 2020): H995—H1007. http://dx.doi.org/10.1152/ajpheart.00269.2020.
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Cytosine-phosphate-guanine (CpG) postconditioning seems to mediate inflammation via Toll-like receptor-1 and Toll-like receptor-9 signaling. Enhanced cytokine and chemokine expressions are partly attenuated by IL-10 and matrix metalloproteinase-8 (MMP8) induction, being associated with lower macrophage infiltration and M1-monocyte differentiation. Furthermore, switch from α- to β-MHC and balanced MMP/TIMP expression led to lesser cardiomyocyte apoptosis, smaller scar size, and preserved cardiac function. Data of pharmacological postconditioning have been widely disappointing to date. Our study suggests a new pathway promoting myocardial postconditioning via Toll-like receptor activation.
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Wang, Jian, and Song-Yuan He. "Effect of ischemic postconditioning on cell apoptosis and expression of relevant genes in non-culprit coronary arteries." Journal of Investigative Medicine 68, no. 7 (August 11, 2020): 1276–81. http://dx.doi.org/10.1136/jim-2020-001328.
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This study was performed to determine the effect of ischemic postconditioning on cell apoptosis and angiotensin II receptor type 1 (AT1), connexin 43 (Cx43), and β-tubulin mRNA expression in non-culprit arteries. Non-culprit arterial tissues were isolated from a rabbit myocardial ischemia-reperfusion model and randomly divided into sham, ischemia-reperfusion, and ischemic postconditioning groups. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Expression of angiotensin II, AT1, Cx43, and β-tubulin mRNA was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). TUNEL analysis indicated significantly higher ratios of apoptotic cells in the ischemia-reperfusion group than in the sham group. However, significantly fewer apoptotic cells were observed in the ischemic postconditioning group than in the ischemia-reperfusion group. The qRT-PCR results indicated significantly higher expression of AT1, Cx43, and β-tubulin mRNA in the ischemia-reperfusion group than in the sham group. However, expression of AT1, Cx43, and β-tubulin was lower in the ischemic postconditioning group than in the ischemia-reperfusion group. The ratios of apoptotic cells and mRNA expression of AT1, Cx43, and β-tubulin in non-culprit arteries were increased after ischemia-reperfusion. Ischemic postconditioning may decrease these features and inhibit the progression of non-culprit arteries.
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Feige, Katharina, Janine Rubbert, Annika Raupach, Martin Stroethoff, André Heinen, Markus W. Hollmann, Ragnar Huhn, and Carolin Torregroza. "Cardioprotective Properties of Mannitol—Involvement of Mitochondrial Potassium Channels." International Journal of Molecular Sciences 22, no. 5 (February 27, 2021): 2395. http://dx.doi.org/10.3390/ijms22052395.
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Cardiac preconditioning (PC) and postconditioning (PoC) are powerful measures against the consequences of myocardial ischemia and reperfusion (I/R) injury. Mannitol—a hyperosmolar solution—is clinically used for treatment of intracranial and intraocular pressure or promotion of diuresis in renal failure. Next to these clinical indications, different organ-protective properties—e.g., perioperative neuroprotection—are described. However, whether Mannitol also confers cardioprotection via a pre- and/or postconditioning stimulus, possibly reducing consequences of I/R injury, remains to be seen. Therefore, in the present study we investigated whether (1) Mannitol-induced pre- and/or postconditioning induces myocardial infarct size reduction and (2) activation of mitochondrial ATP-sensitive potassium (mKATP) channels is involved in cardioprotection by Mannitol. Experiments were performed on isolated hearts of male Wistar rats via a pressure controlled Langendorff system, randomized into 7 groups. Each heart underwent 33 min of global ischemia and 60 min of reperfusion. Control hearts (Con) received Krebs–Henseleit buffer as vehicle only. Pre- and postconditioning was achieved by administration of 11 mmol/L Mannitol for 10 min before ischemia (Man-PC) or immediately at the onset of reperfusion (Man-PoC), respectively. In further groups, the mKATP channel blocker 5HD, was applied with and without Mannitol, to determine the potential underlying cardioprotective mechanisms. Primary endpoint was infarct size, determined by triphenyltetrazolium chloride staining. Mannitol significantly reduced infarct size both as a pre- (Man-PC) and postconditioning (Man-PoC) stimulus compared to control hearts (Man-PC: 31 ± 4%; Man-PoC: 35 ± 6%, each p < 0.05 vs. Con: 57 ± 9%). The mKATP channel inhibitor completely abrogated the cardioprotective effect of Mannitol-induced pre- (5HD-PC-Man-PC: 59 ± 8%, p < 0.05 vs. Man-PC) and postconditioning (5HD-PoC-Man-PoC: 59 ± 10% vs. p < 0.05 Man-PoC). Infarct size was not influenced by 5HD itself (5HD-PC: 60 ± 14%; 5HD-PoC: 54 ± 14%, each ns vs. Con). This study demonstrates that Mannitol (1) induces myocardial pre- and postconditioning and (2) confers cardioprotection via activation of mKATP channels.
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Varga, Zoltán V., Ágnes Zvara, Nóra Faragó, Gabriella F. Kocsis, Márton Pipicz, Renáta Gáspár, Péter Bencsik, et al. "MicroRNAs associated with ischemia-reperfusion injury and cardioprotection by ischemic pre- and postconditioning: protectomiRs." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 2 (July 15, 2014): H216—H227. http://dx.doi.org/10.1152/ajpheart.00812.2013.
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We aimed to characterize early changes in microRNA expression in acute cardioprotection by ischemic pre- and postconditioning in rat hearts. Hearts isolated from male Wistar rats were subjected to 1) time-matched nonischemic perfusion, 2) ischemia-reperfusion (30 min of coronary occlusion and 120 min of reperfusion), 3) preconditioning (3 × 5 min of coronary occlusion) followed by ischemia-reperfusion, or 4) ischemia-reperfusion with postconditioning (6 × 10 s of global ischemia-reperfusion at the onset of reperfusion). Infarct size was significantly reduced by both interventions. Of 350 different microRNAs assessed by microarray analysis, 147–160 microRNAs showed detectable expression levels. Compared with microRNA alterations induced by ischemia-reperfusion versus time-matched nonischemic controls, five microRNAs were significantly affected by both pre- and postconditioning (microRNA-125b*, microRNA-139-3p, microRNA-320, microRNA-532-3p, and microRNA-188), four microRNAs were significantly affected by preconditioning (microRNA-487b, microRNA-139-5p, microRNA-192, and microRNA-212), and nine microRNAs were significantly affected by postconditioning (microRNA-1, microRNA let-7i, microRNA let-7e, microRNA let-7b, microRNA-181a, microRNA-208, microRNA-328, microRNA-335, and microRNA-503). Expression of randomly selected microRNAs was validated by quantitative real-time PCR. By a systematic comparison of the direction of microRNA expression changes in all groups, we identified microRNAs, specific mimics, or antagomiRs that may have pre- and postconditioning-like cardioprotective effects (protectomiRs). Transfection of selected protectomiRs (mimics of microRNA-139-5p, microRNA-125b*, microRNA let-7b, and inhibitor of microRNA-487b) into cardiac myocytes subjected to simulated ischemia-reperfusion showed a significant cytoprotective effect. This is the first demonstration that the ischemia-reperfusion-induced microRNA expression profile is significantly influenced by both pre- and postconditioning, which shows the involvement of microRNAs in cardioprotective signaling. Moreover, by analysis of microRNA expression patterns in cardioprotection by pre- and postconditioning, specific protectomiRs can be revealed as potential therapeutic tools for the treatment of ischemia-reperfusion injury.
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Kocsis, Gabriella F., Judit Pipis, Veronika Fekete, Andrea Kovács-Simon, Louise Odendaal, Éva Molnár, Zoltán Giricz, et al. "Lovastatin interferes with the infarct size-limiting effect of ischemic preconditioning and postconditioning in rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (May 2008): H2406—H2409. http://dx.doi.org/10.1152/ajpheart.00862.2007.
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Statins have been shown to be cardioprotective; however, their interaction with endogenous cardioprotection by ischemic preconditioning and postconditioning is not known. In the present study, we examined if acute and chronic administration of the 3-hydroxy-3-methylglutaryl CoA reductase inhibitor lovastatin affected the infarct size-limiting effect of ischemic preconditioning and postconditioning in rat hearts. Wistar rats were randomly assigned to the following three groups: 1) vehicle (1% methylcellulose per os for 12 days), 2) chronic lovastatin (15 mg·kg−1·day−1 per os for 12 days), and 3) acute lovastatin (1% methylcellulose per os for 12 days and 50 μmol/l lovastatin in the perfusate). Hearts isolated from the three groups were either subjected to a nonconditioning (aerobic perfusion followed by 30-min coronary occlusion and 120-min reperfusion, i.e., test ischemia-reperfusion), preconditioning (three intermittent periods of 5-min ischemia-reperfusion cycles before test ischemia-reperfusion), or postconditioning (six cycles of 10-s ischemia-reperfusion after test ischemia) perfusion protocol. Preconditioning and postconditioning significantly decreased infarct size in vehicle-treated hearts. However, preconditioning failed to decrease infarct size in acute lovastatin-treated hearts, but the effect of postconditioning remained unchanged. Chronic lovastatin treatment abolished postconditioning but not preconditioning; however, it decreased infarct size in the nonconditioned group. Myocardial levels of coenzyme Q9 were decreased in both acute and chronic lovastatin-treated rats. Western blot analysis revealed that both acute and chronic lovastatin treatment attenuated the phoshorylation of Akt; however, acute but not chronic lovastatin treatment increased the phosphorylation of p42 MAPK/ERK. We conclude that, although lovastatin may lead to cardioprotection, it interferes with the mechanisms of cardiac adaptation to ischemic stress.
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Feng, Jianhua, Gregor Fischer, Eliana Lucchinetti, Min Zhu, Lukas Bestmann, David Jegger, Margarete Arras, et al. "Infarct-remodeled Myocardium Is Receptive to Protection by Isoflurane Postconditioning." Anesthesiology 104, no. 5 (May 1, 2006): 1004–14. http://dx.doi.org/10.1097/00000542-200605000-00017.
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Background Postinfarct remodeled myocardium exhibits numerous structural and biochemical alterations. So far, it is unknown whether postconditioning elicited by volatile anesthetics can also provide protection in the remodeled myocardium. Methods Myocardial infarct was induced in male Wistar rats by ligation of the left anterior descending coronary artery. Six weeks later, hearts were buffer-perfused and exposed to 40 min of ischemia followed by 90 min of reperfusion. Anesthetic postconditioning was induced by 15 min of 2.1 vol% isoflurane. In some experiments, LY294002 (15 microM), a phosphatidylinositol 3-kinase inhibitor, was coadministered with isoflurane. Masson's trichrome staining, immunohistochemistry, Western blot analysis, and reverse-transcription polymerase chain reaction served to confirm remodeling. In buffer-perfused hearts, functional recovery was recorded, and acute infarct size was measured using 1% triphenyltetrazolium chloride staining and lactate dehydrogenase release during reperfusion. Western blot analysis was used to determine phosphorylation of reperfusion injury salvage kinases including protein kinase B/Akt and its downstream targets after 15 min of reperfusion. Results Infarct hearts exhibited typical macroscopic and molecular changes of remodeling. Isoflurane postconditioning improved functional recovery and decreased acute infarct size, as determined by triphenyltetrazolium (35 +/- 5% in unprotected hearts vs. 8 +/- 3% in anesthetic postconditioning; P < 0.05) and lactate dehydrogenase release. This protection was abolished by LY294002, which inhibited phosphorylation of protein kinase B/Akt and its downstream targets glycogen synthase kinase 3beta, endothelial nitric oxide synthase, and p70S6 kinase. Conclusions Infarct-remodeled myocardium is receptive to protection by isoflurane postconditioning via protein kinase B/Akt signaling. This is the first time to demonstrate that anesthetic postconditioning retains its marked protection in diseased myocardium.
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Tang, Qi Feng, Yang Xie, Hong Xie, Wen Qiang Jiang, and Zhi Yuan Fang. "Effect of sevoflurane postconditioning on myocardial oncosis and autophagy in ischemia-reperfusion injury in isolated rat heart." Bangladesh Journal of Pharmacology 13, no. 3 (August 28, 2018): 255. http://dx.doi.org/10.3329/bjp.v13i3.36437.
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<p>The effects of sevoflurane postconditioning on myocardial oncosis and autophagy were studied in 32 isolated rat heart of ischemia-reperfusion injury. The hearts were perfused by: a) Sham surgery group, b) simple sevoflurane group, c) simple ischemia-reperfusion group (I/R) group, and d) sevoflurane postconditioning group. The ratios between the gray density values of the target bands to the gray density value of GADPH were used to reflect the Beclin-1, LC3II/I, and porimin expression levels. The LC3II/I level in the sevoflurane postconditioning group was lower than the level in the I/R group. The porimin level in the sevoflurane postconditioning group was lower than the level in the I/R group. The myocardial infarction range in the sevoflurane postconditioning group (33 ± 5%) was significantly diminished compared with the range in the I/R group (53 ± 6%) (p<0.05). Sevoflurane decreased the occurrence of oncosis and alleviated myocardial ischemia-reperfusion injury by inhibiting MPTP opening.</p><p><strong>Video Clip of Methodology:</strong></p><p>14 min 31 sec <a href="https://www.youtube.com/v/i7dssx_6Jsk">Full Screen</a> <a href="https://www.youtube.com/watch?v=i7dssx_6Jsk">Alternate</a></p>
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Yong, Qian Chen, Shiau Wei Lee, Chun Shin Foo, Kay Li Neo, Xin Chen, and Jin-Song Bian. "Endogenous hydrogen sulphide mediates the cardioprotection induced by ischemic postconditioning." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 3 (September 2008): H1330—H1340. http://dx.doi.org/10.1152/ajpheart.00244.2008.
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The present study aimed to investigate the role of hydrogen sulphide (H2S) in the cardioprotection induced by ischemic postconditioning and to examine the underlying mechanisms. Cardiodynamics and myocardial infarction were measured in isolated rat hearts. Postconditioning with six episodes of 10-s ischemia (IPostC) significantly improved cardiodynamic function, which was attenuated by the blockade of endogenous H2S production with d-l-propargylglycine. Moreover, IPostC significantly stimulated H2S synthesis enzyme activity during the early period of reperfusion. However, d-l-propargylglycine only attenuated the IPostC-induced activation of PKC-α and PKC-ε but not that of PKC-δ, Akt, and endothelial nitric oxide synthase (eNOS). These data suggest that endogenous H2S contributes partially to the cardioprotection of IPostC via stimulating PKC-α and PKC-ε. Postconditioning with six episodes of a 10-s infusion of NaHS (SPostC) or 2 min continuous NaHS infusion (SPostC2) stimulated activities of Akt and PKC, improved the cardiodynamic performances, and reduced myocardial infarct size. The blockade of Akt with LY-294002 (15 μM) or PKC with chelerythrine (10 μM) abolished the cardioprotection induced by H2S postconditioning. SPostC2, but not SPostC, also additionally stimulated eNOS. We conclude that endogenous H2S contributes to IPostC-induced cardioprotection. H2S postconditioning confers the protective effects against ischemia-reperfusion injury through the activation of Akt, PKC, and eNOS pathways.