19447

skemik Ön Koşullanma ve Sonradan Koşullanma Mekanizmalarından Biri Olarak Kalsiyum

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

Anahtar Kelimeler:

İskemi, Reperfüzyon, İskemi/Reperfüzyon, İskemik ön koşullanma, Sonradan koşullanma, Kalsiyum

Calcium as One of the Mechanisms of Ischemic Preconditioning and Postconditioning

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

Keywords:

Ischemia, Reperfusion, Ischemia/Reperfusion, Ischemic Preconditioning, Postconditioning, Calcium.,

PDF

___

Murray CE, Jennings RB, Reimer KA: Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation. 1986; 74:1124-1136.
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.
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.
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.
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.
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.
Argaud L, Gateau-Roesch O, Raisky O, Loufouat J, Robert D, Ovize M: Postconditioning inhibits mitochondrial permeability transition. Circulation. 2005; 111:194-197.
Yao Y, Li L, Li L, Gao C, Shi C: Sevoflurane postconditioning protects chronically-infarcted rat hearts against ischemia- reperfusion injury by activation of pro-survival kinases and inhibition of mitochondrial permeability transition pore opening upon reperfusion. Biol Pharm Bull. 2009; 32:1854- 1861.
Şengül İ, Şengül D: İskemik önkoşullanma ve sonradan koşullanma mekanizmaları olarak intraselüler sinyalizasyon ve adenozin. Cumhuriyet Tıp Derg. 2010; 32:127-131.
Tsang A, Hausenloy DJ, Mocanu MM, Yellon DM: Postconditioning: a form of “modified reperfüsion” protects the myocardium by activating the phosphatidylinositol 3- kinase-akt pathway. Circ Res. 2004; 95:230-232.
Bopassa JC, Ferrera R, Gateau-Roesch O, Couture –Lepetit E, Ovize M: PI3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning. Cardiovasc Res. 2006; 69:178-185.
Yang XM, Philipp S, Downey JM, Cohen MV: Postconditioning’s protection is not depended on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanyl cyclase activation. Basic Res Cardiol. 2005; 100:57-63.
Jiang ZS, Wen GB, Tang ZH, Srisakuldee W, Fandrich RR, Kardami E: High molecular weight FGF-2 promotes postconditioning-like cardioprotection linked to activation of the protein kinase C isoforms Akt and p70 S6 kinase. Can J Physiol Pharmacol. 2009; 87:798-804.
Krolikowski JG, Weihrauch D, Bienengraeber M, Kersten JR, Warltier DC, Pagel PS: Role of Erk1/2, p70s6K, and eNOS in isoflurane-induced cardioprotection during early reperfusion in vivo. Can J Anaesth. 2006; 53:174-182.
Yang XM, Downey JM, Cohen MV: Postconditioning’s protection is not depended on circulating blood factors or cells but requires PI3-kinase and guanyl cyclase activation. Cicrulation. 2004; 110;111-168.
Yang X-M, Proctor JB, Cui L, Krieg T, Doney JM, Cohen MV: Multiple brief coronary occlusions during early reperfusion protects rabbit hearts by targeting cell signal pathways. J Am Coll. 2004; 44:1103-1110.
Serviddio G, Venosa N.D, Fedrici A, D’Agostino D, Rollo T, Prigigallo F, Altomare E, Fiore T, Vendemiale G: Brief hypoxia before normoxic reperfusion(postconditioning) protects the heart against ischemia-reperfusion injury by preventing mitochondria peroxyde production and glutathione depletion. FASEB J. 2005; 19,354-361.
Sun YH, Wang NP, Kerendi F, Halkos ME, Kin H, Guyton RA, Vinten-Johansen J, Zhao ZQ: Hypoxic postconditioning reduce cardiomyocyte loss by inhibiting ROS generation and intracelular Ca++ overload. Am J Physiol Heart Circ Physiol. 2005; 4,1900-1908.
Obal D, Dettwiler S, Favoccia C, Scharbatke H, Preckel B, Schlak W: The influence of mitochondrial K-ATP-channels in postconditioning by sevoflurane in the rat in vivo. Anesth Analg. 2005; 101:1252-1260. of preconditioning and
Dosenko NE, Nagibin VS, Tumanovskaya LV, Moibenko AA, Vaage J: Postconditioning prevents apoptotic necrotic and autophagic cell death in culture. Fiziol Zh. 2005; 51:12-17.
Moon JG, Lim HC, Gye MR, Oh JS, Park JW: Postconditioning attenuates ischemia-reperfusion injury in rat skin flap. Microsurgery. 2008; 28:531-537.
Xing B, Chen H, Zhang M, Zhao D, Jiang R, Liu X, Zhang S: Ischemic postconditioning inhibits apoptosis after focal cerebral ischemia/reperfusion injury in the rat. Stroke. 2008; 39:2362-2369.
Serviddio G, Romano AD, Gesualdo L, Tamborra R, Di Palma AM, Rollo T, Altomare E, Vendemiale G: Nephrol Dial Transplant. 2008; 23: 1504-1512.
Santos CH, Gomes OM, Pontes JC, Miiji LN, Bispo MA: The ischemic preconditioning and postconditioning effect on the intestinal ischemia/reperfusion procedure. Acta Cir Bras. 2008; 23: 22- 28. rats undergoing mesenteric
Zaugg M, Lucchinetti E, Spahn DR, Pasch T, Garcia C, Schaub MC: Differential effects of anesthetics on mitochondrial K(ATP) channel activity and cardiomyocyte protection. Anesthesiology. 2002; 97:15-23.
Xu DZ, Lu Q, Kubicka R, Deitch EA: The effect of hypoxia/reoxgenation on the cellular function of intestinal epithelial cells. J Trauma. 1999; 46:280-285.
Meakins JL, Marshall JC: Multiple-organ-failure syndrome. Arch Surg. 1986; 121:196-208.
Li YS, Wang ZX, Li C, Xu M, Li Y, Huang WQ, Xia Z, Liu KX: Proteomics of Ischemia/Reperfusion Injury in Rat Intestine With and Without Ischemic Postconditioning. J Surg Res. Oct 24, 2009 [Epub ahead of print].
Sengul I, Sengul D, Guler O, Hasanoglu A, Urhan MK, Taner AS: Effect of postconditioning on intestinal ischemia- reperfusion injury by inhibiting events in the early minutes of reperfusion in rats. 45th Congress of the European Society for Surgical Research (ESSR), Faculty of Medicine, University of Geneva (Centre Médical Universitaire - CMU), Geneva, Switzerland, 9-12 June 2010. Br J Surg 2010; 94(S4):71-2.
Werns SW, Shea MJ. Lucchesi BR: Free radicals and myocardial injury. Pharmacologic implications. Circulation. 1986; 74:1-5.
Zhou L, Aon MA, Almas T, Cortassa S, Winslow RL, O'Rourke B: A reaction-diffusion model of ROS-induced ROS release in a mitochondrial network. PLoS Comput Biol. 2010. doi: 10.1371/journal.pcbi.1000657
Weisel RD, Mickle DAG,Finkle CD, Tumiati LC, Madonik MM, Ivanov J, Burton GW, Ingold KU: Myocardial free- radical injury after cardioplegia. Circulation. 1989; 80 (suppl 3):14-18.
Busija DW, Gaspar T, Domoki F, Katakam PV, Bari F: Mitochondrial-mediated suppression of ROS production upon exposure of neurons to lethal stress: mitochondrial targeted preconditioning. Adv Drug Deliv Rev. 2008; 60:1471-7.
Hengartner MO: The biochemistry of apoptosis. Nature. 2000; 407:770–776.
Martinou JC, Green DR: Breaking the mitochondrial barrier. Nat Rev Mol Cell Biol. 2001; 2:63–67.
Valko M, Leibfritz D, Moncol J, Cronin MT, Mazur M, Telser J: Free radicals and antioxidants in normal physiological functions and human disease. Int J Biochem Cell Biol. 2007; 39:44–84.
Meldrum DR, Cleveland JC, Rowland RT, Banerjee A, Harken AH: Calcium induced inotrophy is in part mediated by protein kinase C. J Surg Res. 1996; 63:400-413.
Steenbergen C, Fralix T, Murphy E. Role of increased cytosolic calcium concentration myocardial ischemic injury. Basic Res Cardiol. 1993; 88:456-463.
Yu W, Wang JJ, Gan WY, Lin GS, Huang CX: [Effects of verapamil preconditioning on cardiac function in vitro and intracellular free Ca(2+) and L-type calcium current in rat cardiomyocytes post ischemia-reperfusion injury.] Zhonghua Xin Xue Guan Bing Za Zhi. 2010; 38:225-229.
Cohen MV, Yang XM, Downey JM: Acidosis, oxygen, and interference with mitochondrial permeability transition pore formation in the early minutes of reperfusion are critical to postconditioning’s success. Basic Res Cardiol. 2008; 103:464–471.
Hausenloy DJ, Maddock HL, Baxter GF, Yellon DM: Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning? Cardiovasc Res. 2002; 55:534–543.
Heusch G, Boengler K, Schulz R: Inhibition of mitochondrial permeability transition pore opening: the holy grail of cardioprotection. Basic Res Cardiol. 2010; 105:151–154.
Javadov SA, Clarke S, Das M, Griffiths EJ, Lim KH, Halestrap AP: Ischaemic preconditioning inhibits opening of mitochondrial permeability transition pores in the reperfused rat heart. J Physiol. 2003; 549:513–524.