Ischemia-Reperfusion-Induced Injury of Myocardium

Abstract

Serious injuries can be seen on the cells or tissues by the exposure to ischemia or reperfusion after ischemia. Free oxygen radicals, rapidly formed by the influx of molecular oxygen during the period of reperfusion, are the most important factors that are responsible for reperfusion injuries. The most sensitive cellular structures to reperfusion injury are membrane lipids, proteins, nucleic acids and deoxyribonucleic acids. The alterations occured on these structures can cause myocardial stunning, reperfusioninduced arrhythmias, necrosis of myosites, coronary, endothelial and microvasculatory disfunction.

Keywords

• Ischemia, Reperfusion injury, Free Oxygen Radicals, Myocardium

Miyokardiyal İskemi Reperfüzyon Hasarı

Abstract

İskemi veya iskemi sonrası reperfüzyona maruz kalan hücre ya da dokularda ciddi zedelenmeler oluşmaktadır. Reperfüzyon döneminde hücre içine moleküler oksijenin girişiyle hızla oluşan serbest oksijen radikalleri, reperfüzyon hasarında sorumlu tutulan faktörlerin başında gelmektedir. Reperfüzyon hasarına en fazla duyarlı olan hücresel yapılar membran lipidleri, proteinler, nükleik asitler ve deoksiribonükleik asit molekülleridir. Bu yapılarda meydana gelen değişimler sonucunda miyokardiyal sersemleme, reperfüzyon aritmileri, myositlerde nekroz, koroner endotelyal ve mikrovasküler disfonksiyon oluşabilir.

Keywords

• İskemi, Reperfüzyon Hasarı, Serbest Oksijen Radikalleri, Miyokardiyum..

References

1. Damjanov İ, Linder J. Cell injury and cellular adaptations. Anderson’s Pathology. Tenth Edition. Volum 1: 357-365.
2. Kılınç K, Kılınç A. Oksijen toksisitesinin aracı molekülleri olarak oksijen radikalleri. Hacettepe Tıp Dergisi, 2002; 33(2): 110-8.
3. Reilly PM, Schiller HJ, Bulkley GB. Pharmacologic approach to tissue injury mediated by free radicals and other reactive oxygen metabolites. The Am J Off Surgery, 1991;161: 488-503.
4. Granger DN. Role of xanthine oxidaze and granulocytes in ischemia- reperfusion injury. Am J Physiol, 1988; 255: H1269-H1275
5. Barber DA, Harris SR. Oxygen free radicals and antioxidants: a review. Am Pharm, 1994; 9: 26-35.
6. White BC, Grossman LI, Krause GS. Brain injury by global ischemia and reperfusion: a theroretical perspective on membrane damage and repair. Neurology, 1993; 43: 1656-1665.
7. İşlekel H, İşlekel S, Güner G. Biochemical mechanism and tissue injury of cerebral ischemia and reperfusion. URL: http://med.ege.edu.tr/~norolbil/ 2000/NBD09200.html.
8. Rice-Evans CA. Formation of free radicals and mechanisms of action in normal biochemical processes and pathological states. In: Rice-Evans CA, Burdon RH. Free radical damage and its control. England, Elsevier Science Press, 1994; 131-153.

9. Kilgore KS, Lucchesi BR. Reperfusion injury after myocardial infarction: The role of free radicals and the inflammatory response. Clin Biochem, 1993; 26: 359-370.
10. Neves LA, Almeida AP, Khosla MC, Campagnole-Santos MJ, Santos RA. Effect of angiotensin-(1–7) on reperfusion arrhythmias in isolated rat hearts. Braz J Med Biol Res, 1997; 30: 801-809.
11. Xiao CY, Hara A, Yuhki K, et al. Roles of prostaglandin I(2) and thromboxane A(2) in cardiac ischemia–reperfusion injury: a study using mice lacking their respective receptors. Circulation, 2001; 104: 2210-2215.
12. Gross GJ, Kersten JR, Warltier DC. Mechanisms of postischemic contractile dysfunction. Ann Thorac Surg, 1999; 68: 1898- 1904.
13. Moens AL, Claeys MJ, Timmermans JP, Vrints CJ. Myocardial ischemia/reperfusion- injury, a clinical view on a complex pathophysiological process. Int J Cardiol, 2005 Apr 20;100:179-190.
14. Piper HM, Meuter K, MD, Schafer C. Cellular Mechanisms of Ischemia-Reperfusion Injury. Ann Thorac Surg, 2003; 75: 644-648.
15. Kloner RA, Arimie RB, Kay GL, et al. Evidence for stunned myocardium in humans: a 2001 update. Coron Artery Dis, 2001; 12: 349- 356.
16. Heyndrickx GR, Millard RW, McRitchie RJ, Maroko PR, Vatner SF. Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. J Clin Invest, 1975; 56: 978-985.
17. Bolli R. Oxygen-derived free radicals and postischemic myocardial dysfunction (“stunned myocardium”). J Am Coll Cardiol, 1988; 12: 239–249.
18. Kaeffer N, Richard V, Francois A, et al. Preconditioning prevents chronic reperfusion- induced coronary endothelial dysfunction in rats. Am J Physiol, 1996; 271 (3 Pt 2): H842–H849.
19. Viehman GE, Ma XL, Lefer DJ, Lefer AM. Time course of endothelial dysfunction and myocardial injury during coronary arterial occlusion. Am J Physiol, 1991; 261 (3Pt 2): H874–H881.
20. Lefer AM, Lefer DJ. The role of nitric oxide and cell adhesion molecules on the microcirculation in ischaemia–reperfusion. Cardiovasc Res, 1996; 32: 743-751.
21. Kloner RA, Ganote CE, Jennings RB. The “no-reflow” phenomenon after temporary coronary occlusion in the dog. J Clin Invest, 1974; 54: 1496-1508.
22. Kloner RA, Rude RE, Carlson N, et al. Ultrastructural evidence of microvascular damage and myocardial cell injury after coronary artery occlusion: which comes first? Circulation, 1980; 62: 945-952.
23. Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction: pathophysiology and therapy. Circulation, 2000; 101: 2981–2988.
24. Mann JM, Roberts WC. Rupture of the left ventricular free wall during acute myocardial infarction: analysis of 138 necropsy patients and comparison with 50 necropsy patients with acute myocardial infarction without rupture. Am J Cardiol, 1988; 62: 847–859.