Literatura
1.
Radhakrishnan J, Ayoub IM, Grmec Š, Gazmuri RJ. Vitamin-C Compromises Cardiac Resuscitability in a Rat Model
of Ventricular Fibrillation and Closed Chest Resuscitation. Cirucualtion 2010 (in press); Am J Physiol Heart Circ
Physiol 2010 (in press).
2.
Ayoub IM, KolarovaJ, Kantola R, Radhakrishnan J, Wang S, Gazmuri RJ. Zoniporide preserves left ventricular
compliance during VF and minimizes post-resuscitation myocardial dysfunction through benefits on energy
metabolism. CritCare Med 2007;35:2329-36.
3.
Vera JC, Rivas CI, Fischbarg J., Golde DW. Mammalian facilitative hexosetransporters mediate the transport of
dehydroascorbic acid. Nature1993;364:79-82.
4.
KC S, Carcamo JM, Golde DW. Vitamin C enters mitochondria via facilitative glucose transporter 1 (Glut1) and
confers mitochondrial protection against oxidative injury. FASEB J 2005;19:1657-67.
5.
McGown EL, Rusnak MG, Lewis CM, Tillotson JA. Tissue Ascorbic Acid Analysis Using Ferrozine Compared with
the Dinitrophenylhydrazine Method. Anal Biochem 1982 Jan 1; 119(1): 55-61.
6.
Zannoni V, Lynch M, Godstein S, Sato P. A Rapid Micromethod for the Determination of Ascorbic Acid in Plasma
and Tissues. Biochem Med 1974 Sep; 11(1): 41-8.
7.
Sasazuki S, Hayashi T, Nakachi K, Sasaki S, Tsubono Y, Okubo S, Hayashi M, Tsugane S. Protective effect of vitamin
C on oxidative stress: a randomized controlled trial. Int J Vitam Nutr Res 2008;78:121-8.
8.
Halestrap AP, Clarke SJ, Khaliulin I. The role of mitochondria in protection of the heart by preconditioning.
Biochim Biophys Acta 2007;1767(8):1007-31.
9.
Petrosillo G, Di Venosa N, Ruggiero FM et al. Mitchondrial dysfunction associated with cardiac
ischemia/reperfusion can be attenuated by oxygen tension control. Role of oxygen-free radicals and
cardiolipin. Biochem Biophys Acta 2005;1710:78 -86.
10. Juranek I, Bezek S. Controversy of free radical hypothesis: ROS - cause or cosequence of tissue injury. Gen
Physiol Biophys 2005; 24(3):263-78.
11. Kloner RA, Jennings RB. Consequence of brief ischemia: stunning, preconditioning, and their clinical
implications. Circulation 2001; 104(24):2981 -9.
12. Magder S. ROS: toxic molecules or spark of life? Crit Care 2006;10(1):208.
13. Goswami SK,Maulik N, Das DK. Ischemia -reperfusion and cardioprotection: a delicate balance between ROS
and redox homeostasis. Ann Med 2007;39(4):275-89.
14. Starkov AA. The role of mitochondria in reactive oxygen species metabolism and signaling. Ann N Y Acad Sci
2008;1147:37-52.
15. Kaneko M, Hayashi H, Kobayashi A, t al. Stunned myocardium and oxygen free radicals - sarcolemal membrane
damage due to oxygen free radicals. Jpn Circ J. 1991;55(9):885 -9.
16. Bernier M, Hearse DJ, Manning AS. Reperfusion-induced arrhythmias and oxygen-derived free radicals. Studies
with "anti-free radical" interventions and a free radical-generating system in the isolated perfused rat heart. Circ
Res 1986;58:331-40.
17. Manning A, Bernier M, Crome R, et al. Reperfusion-induced arrhythmias: a study of the role of xanthine oxidase-
derived free radicals in the rat heart. J Mol Cell Cardiol 1988;20:35 -45.
18. Yuan G, Kaneko M, Masuda H et al. Decrease in heart mitochondrial creatine kinase activity due to oxygen free
radicals. Biochem Biophys Acta 1992;1140(1):78 -84.
19. 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(1):44-84.
20. Ferdinand P, Schulz R, Baxter GF. Interaction of cardiovascular risk factors with myocardial ischemia/reperfusion
injury,precondition, and postcondition. Pharmacol Rev 2007; 59:418-458
21. Tsutsumi YM, Yokoyama T, Horikawa Y, Roth DM, Patel HH. Reactive oxygen species trigger ischemic and
pharmacological postconditioning: in vivo characterization. Life Sci 2007;81(15):1223-7.
131
URGENTNA MEDICINA - IZBRANA POGLAVJA 2010
prostih kisikovih radikalov nastaja v poprej ishemičnem miokardu v prvih nekaj minutah reperfuzije, kjer
je molekularni kisik izpostavljen redukcijski reakciji in tvorbi prostih kisikovih radikalov kot so:
superoksidni anion, hidroksilni radikali in peroksinitrit. Prosti kisikovi radikali inaktivirajo specifične
encime ali pa sprožijo lipidno peroksidacijo.
Ishemična poškodba povzroči okvaro mitohondrija, s tem pa sproži programirano celično smrt oz.
apoptozo. Pri tem pride do aktivacije B celična levkemija/limfom 2 proteina (B cell leukemia/lymphoma
2, Bcl-2) na zunanji mitohondrijski membrani, ki aktivira protein BAX (Bcl-2 associated X protein, BAX).
Proteini BAX tvorijo pore v mitohondrijski membrani in omogočijo iztekanje citokroma c. Citokrom c se
veže na aktivacijski factor-1 apoptotske proteaze (apoptotic protease-activating factor 1, Apaf-1) in
nastane apoptosom. Apoptosom aktvira encim kaspazo 9, ki sproži kaspazno kaskado s posledično
razgradnjo proteinov, tudi proteinov v mitohondrijski membrani, ki se konča s programirano celično
smrtjo in fagocitozo celice.
Do'stlaringiz bilan baham: |