Journals / Düzce Tıp Fakültesi Dergisi / 2012 / Cilt: 14 Sayı: 3

Calcium as One of the Mechanisms of Ischemic Preconditioning and Postconditioning

skemik Ön Koşullanma ve Sonradan Koşullanma Mekanizmalarından Biri Olarak Kalsiyum

Pages
74–79
Publication Date
2012-12-01
DOI
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

It is thoughtthat, Ca++holds an important place in those potential mechanisms

📌 3 Key Takeaways

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Objective & Hypothesis:After the endogenous phenomenon of “ischemic preconditioning” in which repetitive briefepisodes of ischemia render the myocardium more resistant to subsequent prolonged ischemicinsult; in recent years, the protection via a similiar regimen of brief episodes of ischemia carriedout “just after”, instead of “just before” the maintained ischemia was determined as“postconditioning”.High levels of Ca++are blamed for fatal injury of cells that underwent to ischemia-reperfusionand their postischemic dysfunction.
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Key Findings & Data:Besides, the main reason of cell dysfunction is dependenton ischemia-reperfusion and cell death are stressed on as “intracellular Ca++overloading”.However; it was showed that, paradoxal elevations of Ca++levels in a short interval protectsthe tissue from the more serious elevations of it.Though the protective mechanisms of ischemic preconditioning and postconditioning are notclearly known yet, lots of the potential mechanisms had been blaming up to date.
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Conclusion & Impact:It is thoughtthat, Ca++holds an important place in those potential mechanisms
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:İskemi · Reperfüzyon · İskemi/Reperfüzyon

Abstract

After the endogenous phenomenon of “ischemic preconditioning” in which repetitive briefepisodes of ischemia render the myocardium more resistant to subsequent prolonged ischemicinsult; in recent years, the protection via a similiar regimen of brief episodes of ischemia carriedout “just after”, instead of “just before” the maintained ischemia was determined as“postconditioning”.High levels of Ca++are blamed for fatal injury of cells that underwent to ischemia-reperfusionand their postischemic dysfunction. Besides, the main reason of cell dysfunction is dependenton ischemia-reperfusion and cell death are stressed on as “intracellular Ca++overloading”.However; it was showed that, paradoxal elevations of Ca++levels in a short interval protectsthe tissue from the more serious elevations of it.Though the protective mechanisms of ischemic preconditioning and postconditioning are notclearly known yet, lots of the potential mechanisms had been blaming up to date. It is thoughtthat, Ca++holds an important place in those potential mechanisms

Özet

Önceki kısa süreli tekrarlayan iskemi-reperfüzyon dönemlerinin, miyokardiyumu, daha sonrakiasıl iskemi-reperfüzyon hasarına karşı daha dirençli hale getirdiği ve koruyucu etkisi olduğugösterilen endojen fenomen “iskemik ön koşullanma”dan sonra; son yıllarda, benzer bir rejimle,maruz kalınan iskemiden “hemen önce” yerine, “hemen sonra” kısa süreli tekrarlayan iskemireperfüzyon epizodlarının uygulanması ile oluşan koruyuculuk ise “sonradan-koşullanma”olarak tanımlanmıştır.İskemi-reperfüzyona uğramış hasarlı hücrelerdeki ölümcül hasardan ve bunların postiskemikdisfonksiyonundan, yüksek Ca++konsantrasyonu sorumlu tutulmakta ve iskemi-reperfüzyonabağlı hücre disfonksiyonu ve ölümünün asıl nedeni olarak “intrasellüler Ca++yüklenmesi”gösterilmektedir. Bununla birlikte, kısa süreli Ca++paradoks yükselmesinin dokuyu daha ciddiCa++yükselmelerinden koruduğu da bildirilmiştir.İÖ ve SK’nın koruyucu mekanizmaları henüz tam olarak bilinmemekle birlikte, bugüne dekpotansiyel birçok mekanizma suçlanmıştır. Ca++’ un bu mekanizmalar içinde önemli bir yertuttuğu düşünülmektedir

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Cite This Article

ŞENGÜL, D., ŞENGÜL, İ. (2012). Calcium as One of the Mechanisms of Ischemic Preconditioning and Postconditioning. Düzce Tıp Fakültesi Dergisi, Cilt: 14 Sayı: 3, 74–79. https://ajindex.com/articles/927170

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References (7)

  1. Murray CE, Jennings RB, Reimer KA: Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation. 1986; 74:1124-1136.
  2. Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA, Vinten-Johansen J: Inhibition of myocardial injury reperfusion:comparison with ischemic preconditioning. Am J Physiol. 2003; 285: H579-H588. during Mei DA, Elliott GT, Gross GJ: KATP channels mediate late preconditioning monophosphoryl lipid A. Am J Physiol. 1996; 271: H2723- H2729. infarction produced by Sengul I, Sengul D: Potasyum–ATP kanalları ve reperfüzyon hasarı azaltıcı koşullanmalar. Nobel Med. Nobel Med. 2010. 6:112. Harun E, Dursun D, Ender S: İskemik önkoşullanma. Anadolu Kardiyol Derg. 2003; 3,144-149. Armstrong SC: Protein kinase activation and myocardial ischemia- reperfusion injury. Cardiovasc Res. 2004; 61:427- 436. Murphy E: Pimary and secondary signaling pathways in early preconditioning converge in mitochondria to produce cardioprotection. Circ Res. 2004; 94: 7-16.
  3. Stumpner J, Redel A, Kellermann A, Lotz CA, Blomeyer CA, Smul TM, Kehl F, Roewer N, Lange M.:Differential role of Pim-1 kinase in anesthetic-induced and ischemic preconditioning Anesthesiology. 2009; 111:1257-1264. myocardial infarction. Sadat U: Signaling pathways of cardioprotective ischemic preconditioning. Int J Surg. 2009; 7:490-498.
  4. Xuan YT, Guo Y, Zhu Y, Wang OL, Rokosh G, Messing RO, Bolli R: Role of the protein kinase C-epsilon-Raf-1-MEK- 1/2-p44/42 MAPK signaling cascade in the activation of signal transducers and activators of transcription 1 and 3 and induction preconditioning. Circulation. 2005; 112: 1971-1978. after ischemic Downey JM, Cohen MV: Arguments is favor of protein kinase C playing an important role in ischemic preconditioning. Basic Res Cardiol. 1997; 92: 37-39. Nishizuka Y: Intracellular signalling by hydrolysisof phospholipids and activation of protein kinase C. Science. 1992; 258:607-610.
  5. Krieg T, Qin Q, Philipp S, Alexeyev MF, Cohen MV, Downey JM: Acetylcholine and bradykinin trigger preconditioning in the heart through a pathway that includes Akt and NOS. Am J Physiol Heart Circ Physiol. 2004; 287: 2606-2611.
  6. Tsang A, Hausenley DJ, Mocanu MM, Yellon DM: Postconditioning: a form of “modified reperfusion” protects myocardium by activating Phosphatidylinositol 3-kinase-Akt pathway. Circ Res. 2004; 95:230-232.
  7. Argaud L, Gateau-Roesch O, Raisky O, Loufouat J, Robert D, Ovize M: Postconditioning inhibits mitochondrial permeability transitio