The co-application of hypoxic preconditioning and postconditioning abolishes their own protective effect on systolic function in human myocardium

Roleder, Tomasz; Gołba, Krzysztof S.; Kunecki, Marcin; Malinowski, Marcin; Biernat, Jolanta; Smołka, Grzegorz; Deja, Marek

doi:10.5603/cj.2013.0131

Cited by 5 publications

(6 citation statements)

References 29 publications

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“…Nonetheless, the validity of this argument could be challenged, since it has been reported in the skeletal muscle of rats subjected to ischemia and reperfusion that the combination of IPreC and IPostC reduced glycogen depletion to a degree similar to that of IPreC alone whilst IPostC alone did not show protection [34]. Other investigators have observed a loss of protection in the human right atrial myocardium with the co-application of IPreC and IPostC [35]. Differences in the protocol and the animal model used may explain the discrepancy between these results but, certainly, this is an area of great clinical interest that would require further investigations.…”

Section: Discussionmentioning

confidence: 99%

Ischemic postconditioning of the isolated human myocardium: Role of the applied protocol

Casós

Pérez

Blasco-Lucas

et al. 2015

IJC Heart & Vasculature

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BackgroundIschemic postconditioning (IPostC), has been proposed as a useful approach to reduce infarct size in all species, but its clinical utility remains unclear.ObjectiveTo investigate the role played by the protocol used on the efficacy of IPostC in protecting the diseased human myocardium.MethodsMyocardial atrial samples from patients were subjected to a 90 min ischemia/120 min reoxygenation followed by different IPostC protocols to investigate the role of the time of ischemia (30, 60, 90 and 120 s) and the number of cycles (1, 2, 3 and 4) with 60 and 120 s of total ischemic time. Muscles were also subjected to ischemic preconditioning (IPreC). The release of lactate dehydrogenase (LDH) and the measurement of tetrazolium bromide (MTT) were determined.ResultsIPostC increased the LDH and decreased the MTT values from those of control, independently of the duration of the conditioning ischemia. LDH and MTT values also worsened by augmenting the number of IPostC cycles whereas they were significantly improved by IPreC. However, analysis of individual results indicated that in approximately 1/3 of the cases IPostC exhibited some degree of protection especially in the presence of increased ischemic injury.ConclusionsThe present findings show that IPostC of the human myocardium may be influenced by the protocol used and also by the degree of the preceding ischemic injury. IPostC was beneficial in approximately 1/3 of the cases; however in the remaining cases it increased ischemic damage and, therefore, these results raise a word of caution on its broad clinical use.

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Section: Discussionmentioning

confidence: 99%

Ischemic postconditioning of the isolated human myocardium: Role of the applied protocol

Casós

Pérez

Blasco-Lucas

et al. 2015

IJC Heart & Vasculature

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“…Mitochondrial ATP-sensitive potassium channels (mKATP) control the activity of the mPTPs [13]. NO in low concentration was documented to be a potent mKATP opener through activation of anti-apoptotic cascade of enzymes called RISK pathway [14][15][16][17].…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide signaling in the ischemic postconditioning of human heart muscle (RCD code: III)

Kunecki

Płazak

Podolec

et al. 2016

Journal of Rare Cardiovascular Diseases

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Background: Ischemic heart conditioning is well documented to trigger the intrinsic protective mechanisms of resistance against ischemia/reperfusion (I/R) injury. Previous studies on animal model have suggested that the nitric oxide (NO) mediates the beneficial effect of ischemic postconditioning (POC). We tested the hypothesis that POC provide cardioprotection in the NO-dependent mechanism in the human myocardium. Methods: Human atrial trabeculae were subjected to simulated I/R injury. To achieve POC triple brief hypoxia periods were followed by the lethal hypoxia. Non-selective inhibitor of NO synthase: NG-monomethyl-L-arginine (L-NMMA) was used at the time of re-oxygenation in the POC protocol. Contractility of the myocardium was assessed as the maximal force of a contraction (Amax), the rate of rise of the force of a contraction (Slope L) and cardiac muscle relaxation -as the rate of decay of the force of a contraction (Slope T). Results: Co-application of L-NMMA with POC resulted in the decrease of Amax, Slope L and Slope T during re-oxygenation period as compared to POC only. Conclusions: At re-oxygenation period, the blockade of NO synthesis has deleterious effect on systolic and diastolic function of human myocardium, as well as attenuates the beneficial effect of ischemic POC. JRCD 2016; 2 (6): 181-184

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“…Сходные данные получили T. Roleder и соавт. [27]. Трабекулу, изолированную из правого предсердия человека, они подвергали воздей-ствию гипоксии (60 мин) и реоксигенации (60 мин) [27].…”

Section: данные экспериментов на изолированных препаратах сердца челоunclassified

“…[27]. Трабекулу, изолированную из правого предсердия человека, они подвергали воздей-ствию гипоксии (60 мин) и реоксигенации (60 мин) [27]. Тяжи соединительной ткани были получены во время операции АКШ у пациентов, средний возраст которых составлял 60 лет.…”

Section: данные экспериментов на изолированных препаратах сердца челоunclassified

“…В группу контроля были включены трабекулы с гипоксией-реоксигенацией без адаптации к реоксигенации. Авторы установили, что сила сокращений посткондиционированных структур во время реоксиге-нации была выше, чем в контроле [27]. Эти данные гово-рят о том, что феномен посткондиционирования можно реализовать на изолированных трабекулах предсердия больных ишемической болезнью сердца.…”

Section: данные экспериментов на изолированных препаратах сердца челоunclassified

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Postconditioning the Heart: Analysis of Experimental and Clinical Data

Maslov¹,

Николаевич²,

Tsibulnikov³

et al. 2016

Annals RAMS

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В 2003 г. группа американских физиологов открыла феномен, который они назвали «ишемическим постконди-ционированием» (ischemic postconditioning) [1]. Суть фено-мена сводится к тому, что миокард становится устойчивым к реперфузионным повреждениям, если после длительного снижения кровоснабжения в течение нескольких сеансов сердце попеременно подвергают кратковременному воз-обновлению (не более 1 мин) и нарушению (не более 1 мин) тока крови: по сути, речь идет об адаптации к реперфузии на уровне сердца. Вслед за этой работой появилось мно-го публикаций, посвященных рецепторному и сигналь-ному механизму посткондиционирования. Большинство исследований было выполнено на молодых животных без сопутствующей патологии. Между тем многие пациенты, которым выполняется кардиохирургическое вмешатель-ство, -люди пожилого возраста с атеросклерозом коронар-ных сосудов, зачастую с сахарным диабетом и артериальной гипертензией [2]. Этот факт послужил причиной проведе-ния исследований по посткондиционированию на живот-ных с экспериментальной сопутствующей патологией. L.N. Maslov

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The co-application of hypoxic preconditioning and postconditioning abolishes their own protective effect on systolic function in human myocardium

Cited by 5 publications

References 29 publications

Ischemic postconditioning of the isolated human myocardium: Role of the applied protocol

Ischemic postconditioning of the isolated human myocardium: Role of the applied protocol

Nitric oxide signaling in the ischemic postconditioning of human heart muscle (RCD code: III)

Postconditioning the Heart: Analysis of Experimental and Clinical Data

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