Yıl: 2021 Cilt: 27 Sayı: 3 Sayfa Aralığı: 179 - 190 Metin Dili: Türkçe DOI: 10.5505/tbdhd.2021.83435 İndeks Tarihi: 12-07-2022

İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW

Öz:
İskemik inme sonrası tıkanan büyük damarın geri açılmasına dayanan rekanalizasyon tedavileri günümüzdeki tek tedavi seçeneğidir ve klinik fonksiyonu iyileştirmede önemli ilerlemeler sağlamıştır. Ancak rekanalizasyon sağlanması her zaman doku sağ kalımı ve olumlu fonksiyonel iyileşme ile sonlanmamaktadır. Bu uyumsuzluğun altında yatan çeşitli nedenlerden bir tanesi “no-reflow” fenomenidir. Bu terim ilk olarak kardiyoloji literatüründe rekanalizasyon sağlanmasına rağmen parankimal dokuda reperfüzyon sağlanamaması durumunu tarif etmek için kullanılmıştır. Takip eden dönemde deneysel iskemik inme modellerinde, tıkalı büyük damarların açılmasına karşın kan akımının mikrodolaşım düzeyinde düzelmemesi ile seyreden benzer bir sürecin varlığı kanıtlanmıştır. Uzun yıllardır deneysel çalışmalarda varlığı bilinen ancak patofizyolojisi tam olarak aydınlatılamayan bu fenomenin nedenlerinden bazıları kan elemanlarının aggregasyonu, kan vizkositesinde artma, nörovasküler ünite hücrelerinden perisitlerin kasılarak mikrodamarları daraltması, inflamatuar süreçlerin aktifleşmesidir. Bu fenomen, rekanalizasyon tedavilerinin başarısının istenen düzeyde olamamasına neden olduğundan özellikle klinik çalışmalarla patofizyolojisinin tam olarak aydınlatılması gereklidir. İskemik inmede rekanalizayon tedavisi yanında reperfüzyonu iyileştirmeye yönelik kokteyl tedavileri “no-reflow’’ fenomenini önleyebilir.
Anahtar Kelime:

THE MYSTERIOUS PHENOMENON OF ISCHEMIC STROKE: NO-REFLOW

Öz:
Recanalization therapies based on reopening of the occluded great vessel after ischemic stroke are the only treatment options available today and have made significant advances in improving clinical function. However, providing recanalization does not always result in tissue survival and positive functional recovery. One of the various reasons underlying this incompatibility is the "no-reflow" phenomenon. This term was first used in the cardiology literature to describe the situation in which parenchymal tissue reperfusion was not achieved despite recanalization. In the following period, the existence of a similar process in experimental ischemic stroke models, in which the blood flow did not improve at the microcirculation level despite the opening of the occluded great vessels, was proven. Some of the causes of this phenomenon, which has been known in experimental studies for many years but whose pathophysiology has not been fully elucidated, are the aggregation of blood elements, increase in blood viscosity, contraction of pericytes -a component of neurovascular unit, narrowing of microvessels, and activation of inflammatory processes. Since this phenomenon causes the success of recanalization treatments not to be at the desired level, its pathophysiology should be fully elucidated, especially through clinical studies. Cocktail therapies to improve reperfusion besides recanalization therapy in ischemic stroke can prevent the "no-reflow" phenomenon.
Anahtar Kelime:

Belge Türü: Makale Makale Türü: Derleme Erişim Türü: Erişime Açık
  • 1. Feigin VL, Forouzanfar MH, Krishnamurthi R, et al. Global and regional burden of stroke during 1990-2010: Findings Türk Beyin Damar Hastalıkları Dergisi 2021; 27(3): 179-190 from the global burden of disease study 2010. Lancet 2014; 383(9913): 245-254.
  • 2. Ames A, 3rd, Wright RL, Kowada M, et al. Cerebral ischemia. Ii. The no-reflow phenomenon. Am J Pathol 1968; 52(2): 437-453.
  • 3. Chiang J, Kowada M, Ames A, 3rd, et al. Cerebral ischemia. Iii. Vascular changes. Am J Pathol 1968; 52(2): 455-476.
  • 4. Little JR, Kerr FW, Sundt TM, Jr. Microcirculatory obstruction in focal cerebral ischemia: An electron microscopic investigation in monkeys. Stroke 1976; 7(1): 25-30.
  • 5. Zhang ZG, Chopp M, Goussev A, et al. Cerebral microvascular obstruction by fibrin is associated with upregulation of pai-1 acutely after onset of focal embolic ischemia in rats. J Neurosci 1999; 19(24): 10898-10907.
  • 6. Yemisci M, Gursoy-Ozdemir Y, Vural A, et al. Pericyte contraction induced by oxidative-nitrative stress impairs capillary reflow despite successful opening of an occluded cerebral artery. Nat Med 2009; 15(9): 1031-1037.
  • 7. Fischer EG, Ames 3d A. Studies on mechanisms of impairment of cerebral circulation following ischemia: Effect of hemodilution and perfusion pressure. Stroke 1972; 3(5): 538-542.
  • 8. Crowell JW, Sharpe, SP, LrAucht, RL, et al. Echanism of death after resuscitation following acute circulatory arrest. Surgery 1955; 38.
  • 9. Neely WA, and Youmans, J. R. Anoxia of canine brain without damage. JAMA 1963; 183: 1085-1087.
  • 10. Sheehan HL, Davis JC. Patchy permanent renal ischæmia. The Journal of Pathology and Bacteriology 1959; 77(1): 33- 48.
  • 11. Krug A, Du Mesnil de R, Korb G. Blood supply of the myocardium after temporary coronary occlusion. Circ Res 1966; 19(1): 57-62.
  • 12. Kloner RA, Ganote CE, Jennings RB. The "no-reflow" phenomenon after temporary coronary occlusion in the dog. J Clin Invest 1974; 54(6): 1496-1508.
  • 13. de la Torre JC, Fortin T, Saunders JK, et al. The no-reflow phenomenon is a post-mortem artifact. Acta Neurochir (Wien) 1992; 115(1-2): 37-42.
  • 14. del Zoppo GJ, Schmid-Schonbein GW, Mori E, et al. Polymorphonuclear leukocytes occlude capillaries following middle cerebral artery occlusion and reperfusion in baboons. Stroke 1991; 22(10): 1276-1283.
  • 15. Mori E, del Zoppo GJ, Chambers JD, et al. Inhibition of polymorphonuclear leukocyte adherence suppresses no- reflow after focal cerebral ischemia in baboons. Stroke 1992; 23(5): 712-718.
  • 16. Liu S, Connor J, Peterson S, et al. Direct visualization of trapped erythrocytes in rat brain after focal ischemia and reperfusion. J Cereb Blood Flow Metab 2002; 22(10): 1222- 1230.
  • 17. del Zoppo GJ, Mabuchi T. Cerebral microvessel responses to focal ischemia. J Cereb Blood Flow Metab 2003; 23(8): 879- 894.
  • 18. McHedlishvili GI, Ormotsadze LG, Nikolaishvili LS, et al. Reaction of different parts of the cerebral vascular system in asphyxia. Experimental Neurology 1967; 18(2): 239-252.
  • 19. Hall CN, Reynell C, Gesslein B, et al. Capillary pericytes regulate cerebral blood flow in health and disease. Nature 2014; 508(7494): 55-60.
  • 20. Alarcon-Martinez L, Yilmaz-Ozcan S, Yemisci M, et al. Capillary pericytes express alpha-smooth muscle actin, which requires prevention of filamentous-actin depolymerization for detection. Elife 2018; 7. Türk Beyin Damar Hastalıkları Dergisi 2021; 27(3): 179-190
  • 21. Armulik A, Genove G, Betsholtz C. Pericytes: Developmental, physiological, and pathological perspectives, problems, and promises. Dev Cell 2011; 21(2): 193-215.
  • 22. Dalkara T, Gursoy-Ozdemir Y, Yemisci M. Brain microvascular pericytes in health and disease. Acta Neuropathol 2011; 122(1): 1-9.
  • 23. KW. Z. Der feinere bau der blutcapillares. Anat Entwickl 1923; 68: 29 - 109.
  • 24. Le Beux YJ WJ. Actin- and myosin-like filaments in rat brain pericytes. Anat Rec 1978; 190: 811 - 826.
  • 25. Joyce NC HM, Palade GE. Contractile proteins in pericytes. Immunoperoxidase localization of topomyosin. Cell Biol 1985; 100: 1379 - 1386.
  • 26. Toribatake Y, Tomita K, Kawahara N, et al. Regulation of vasomotion of arterioles and capillaries in the cat spinal cord: Role of alpha actin and endothelin-1. Spinal Cord 1997; 35(1): 26-32.
  • 27. Matsugi T, Chen Q, Anderson DR. Contractile responses of cultured bovine retinal pericytes to angiotensin ii. Arch Ophthalmol 1997; 115(10): 1281-1285.
  • 28. Dodge AB, Hechtman HB, Shepro D. Microvascular endothelial-derived autacoids regulate pericyte contractility. Cell Motil Cytoskeleton 1991; 18(3): 180-188.
  • 29. Horlyck S, Cai C, Helms HCC, et al. Atp induces contraction of cultured brain capillary pericytes via activation of p2y- type purinergic receptors. Am J Physiol Heart Circ Physiol 2021; 320(2): H699-H712.
  • 30. Nortley R, Korte N, Izquierdo P, et al. Amyloid beta oligomers constrict human capillaries in alzheimer's disease via signaling to pericytes. Science 2019; 365(6450).
  • 31. Nelson AR, Sagare MA, Wang Y, et al. Channelrhodopsin excitation contracts brain pericytes and reduces blood flow in the aging mouse brain in vivo. Front Aging Neurosci 2020; 12: 108.
  • 32. Hill RA, Tong L, Yuan P, et al. Regional blood flow in the normal and ischemic brain is controlled by arteriolar smooth muscle cell contractility and not by capillary pericytes. Neuron 2015; 87(1): 95-110.
  • 33. Kureli G, Yilmaz-Ozcan S, Erdener SE, et al. F-actin polymerization contributes to pericyte contractility in retinal capillaries. Exp Neurol 2020; 332: 113392.
  • 34. Alarcon-Martinez L, Yilmaz-Ozcan S, Yemisci M, et al. Retinal ischemia induces alpha-sma-mediated capillary pericyte contraction coincident with perivascular glycogen depletion. Acta Neuropathol Commun 2019; 7(1): 134.
  • 35. Taskiran-Sag A, Yemisci M, Gursoy-Ozdemir Y, et al. Improving microcirculatory reperfusion reduces parenchymal oxygen radical formation and provides neuroprotection. Stroke 2018; 49(5): 1267-1275.
  • 36. Atochin DN, Wang A, Liu VW, et al. The phosphorylation state of enos modulates vascular reactivity and outcome of cerebral ischemia in vivo. J Clin Invest 2007; 117(7): 1961- 1967.
  • 37. Iadecola C, Anrather J. The immunology of stroke: From mechanisms to translation. Nat Med 2011; 17(7): 796-808.
  • 38. El Amki M, Gluck C, Binder N, et al. Neutrophils obstructing brain capillaries are a major cause of no-reflow in ischemic stroke. Cell Rep 2020; 33(2): 108260.
  • 39. Perez-de-Puig I, Miro-Mur F, Ferrer-Ferrer M, et al. Neutrophil recruitment to the brain in mouse and human ischemic stroke. Acta Neuropathol 2015; 129(2): 239-257.
  • 40. Quenault A, Martinez de Lizarrondo S, Etard O, et al. Molecular magnetic resonance imaging discloses endothelial activation after transient ischaemic attack. Brain 2017; 140(1): 146-157.
  • 41. Reglero-Real N, Colom B, Bodkin JV, et al. Endothelial cell junctional adhesion molecules: Role and regulation of expression in inflammation. Arterioscler Thromb Vasc Biol 2016; 36(10): 2048-2057.
  • 42. Krueger M, Bechmann I, Immig K, et al. Blood-brain barrier breakdown involves four distinct stages of vascular damage in various models of experimental focal cerebral ischemia. J Cereb Blood Flow Metab 2015; 35(2): 292-303.
  • 43. Khatri R, McKinney AM, Swenson B, et al. Blood-brain barrier, reperfusion injury, and hemorrhagic transformation in acute ischemic stroke. Neurology 2012; 79(13 Suppl 1): S52-57.
  • 44. Fischer EG, Ames A, 3rd, Hedley-Whyte ET, et al. Reassessment of cerebral capillary changes in acute global ischemia and their relationship to the "no-reflow phenomenon". Stroke 1977; 8(1): 36-39.
  • 45. Garcia JH, Liu KF, Yoshida Y, et al. Brain microvessels: Factors altering their patency after the occlusion of a middle cerebral artery (wistar rat). Am J Pathol 1994; 145(3): 728-740.
  • 46. Chen H, Chopp M, Schultz L, et al. Sequential neuronal and astrocytic changes after transient middle cerebral artery occlusion in the rat. J Neurol Sci 1993; 118(2): 109-106.
  • 47. Kempski O, Staub F, Jansen M, et al. Molecular mechanisms of glial cell swelling in acidosis. Adv Neurol 1990; 52: 39- 45.
  • 48. Noble LJ, Hall JJ, Chen S, et al. Morphologic changes in cultured astrocytes after exposure to glutamate. J Neurotrauma 1992; 9(3): 255-267.
  • 49. Mishra A, Reynolds JP, Chen Y, et al. Astrocytes mediate neurovascular signaling to capillary pericytes but not to arterioles. Nat Neurosci 2016; 19(12): 1619-1627.
  • 50. Biesecker KR, Srienc AI, Shimoda AM, et al. Glial cell calcium signaling mediates capillary regulation of blood flow in the retina. J Neurosci 2016; 36(36): 9435-9445.
  • 51. del Zoppo GJ. Acute anti-inflammatory approaches to ischemic stroke. Ann N Y Acad Sci 2010; 1207: 143-148.
  • 52. Leao AA. Further observations on the spreading depression of activity in the cerebral cortex. J Neurophysiol 1947; 10(6): 409-414.
  • 53. Somjen GG. Mechanisms of spreading depression and hypoxic spreading depression-like depolarization. Physiol Rev 2001; 81(3): 1065-1096.
  • 54. Charles AC, Baca SM. Cortical spreading depression and migraine. Nat Rev Neurol 2013; 9(11): 637-644.
  • 55. Ayata C, Lauritzen M. Spreading depression, spreading depolarizations, and the cerebral vasculature. Physiol Rev 2015; 95(3): 953-993.
  • 56. Dreier JP, Petzold G, Tille K, et al. Ischaemia triggered by spreading neuronal activation is inhibited by vasodilators in rats. J Physiol 2001; 531(Pt 2): 515-526.
  • 57. Ayata C, Shin HK, Salomone S, et al. Pronounced hypoperfusion during spreading depression in mouse cortex. J Cereb Blood Flow Metab 2004; 24(10): 1172- 1182.
  • 58. Busija DW, Meng W. Retention of cerebrovascular dilation after cortical spreading depression in anesthetized rabbits. Stroke 1993; 24(11): 1740-1744; discussion 1744-1745.
  • 59. Chuquet J, Hollender L, Nimchinsky EA. High-resolution in vivo imaging of the neurovascular unit during spreading depression. J Neurosci 2007; 27(15): 4036-4044.
  • 60. Duckrow RB. Regional cerebral blood flow during spreading cortical depression in conscious rats. J Cereb Blood Flow Metab 1991; 11(1): 150-154. İskemik inmede no-reflow
  • 61. Obrenovitch TP, Chen S, Farkas E. Simultaneous, live imaging of cortical spreading depression and associated cerebral blood flow changes, by combining voltage- sensitive dye and laser speckle contrast methods. Neuroimage 2009; 45(1): 68-74.
  • 62. Nedergaard M, Hansen AJ. Characterization of cortical depolarizations evoked in focal cerebral ischemia. J Cereb Blood Flow Metab 1993; 13(4): 568-574.
  • 63. Luckl J, Dreier JP, Szabados T, et al. Peri-infarct flow transients predict outcome in rat focal brain ischemia. Neuroscience 2012; 226: 197-207.
  • 64. Bere Z, Obrenovitch TP, Kozak G, et al. Imaging reveals the focal area of spreading depolarizations and a variety of hemodynamic responses in a rat microembolic stroke model. J Cereb Blood Flow Metab 2014; 34(10): 1695- 1705.
  • 65. Kao YC, Li W, Lai HY, et al. Dynamic perfusion and diffusion mri of cortical spreading depolarization in photothrombotic ischemia. Neurobiol Dis 2014; 71: 131- 139.
  • 66. Wade JG, Amtorp O, Sorensen SC. No-flow state following cerebral ischemia. Role of increase in potassium concentration in brain interstitial fluid. Arch Neurol 1975; 32(6): 381-384.
  • 67. Shin HK, Dunn AK, Jones PB, et al. Vasoconstrictive neurovascular coupling during focal ischemic depolarizations. J Cereb Blood Flow Metab 2006; 26(8): 1018-1030.
  • 68. Yemisci M, Eikermann-Haerter K. Aura and stroke: Relationship and what we have learnt from preclinical models. J Headache Pain 2019; 20(1): 63.
  • 69. Takano T, Tian GF, Peng W, et al. Astrocyte-mediated control of cerebral blood flow. Nat Neurosci 2006; 9(2): 260-267.
  • 70. Yuzawa I, Sakadzic S, Srinivasan VJ, et al. Cortical spreading depression impairs oxygen delivery and metabolism in mice. J Cereb Blood Flow Metab 2012; 32(2): 376-386.
  • 71. Nakamura H, Strong AJ, Dohmen C, et al. Spreading depolarizations cycle around and enlarge focal ischaemic brain lesions. Brain 2010; 133(Pt 7): 1994-2006.
  • 72. Strong AJ, Harland SP, Meldrum BS, et al. The use of in vivo fluorescence image sequences to indicate the occurrence and propagation of transient focal depolarizations in cerebral ischemia. J Cereb Blood Flow Metab 1996; 16(3): 367-377.
  • 73. Dohmen C, Sakowitz OW, Fabricius M, et al. Spreading depolarizations occur in human ischemic stroke with high incidence. Ann Neurol 2008; 63(6): 720-728.
  • 74. Gaudin A, Yemisci M, Eroglu H, et al. Squalenoyl adenosine nanoparticles provide neuroprotection after stroke and spinal cord injury. Nat Nanotechnol 2014; 9(12): 1054- 1062.
  • 75. Choudhri TF, Hoh BL, Zerwes HG, et al. Reduced microvascular thrombosis and improved outcome in acute murine stroke by inhibiting gp iib/iiia receptor-mediated platelet aggregation. J Clin Invest 1998; 102(7): 1301-1310.
  • 76. Ishikawa M, Vowinkel T, Stokes KY, et al. Cd40/cd40 ligand signaling in mouse cerebral microvasculature after focal ischemia/reperfusion. Circulation 2005; 111(13): 1690- 1696.
  • 77. Alarcon-Martinez L, Yemisci M, Dalkara T. Pericyte morphology and function. Histol Histopathol 2021; 36(6): 633-643.
  • 78. Enlimomab Acute Stroke Trial I. Use of anti-icam-1 therapy in ischemic stroke: Results of the enlimomab acute stroke Türk Beyin Damar Hastalıkları Dergisi 2021; 27(3): 179-190 trial. Neurology 2001; 57(8): 1428-1434.
  • 79. Adams HP, Jr., Effron MB, Torner J, et al. Emergency administration of abciximab for treatment of patients with acute ischemic stroke: Results of an international phase iii trial: Abciximab in emergency treatment of stroke trial (abestt-ii). Stroke 2008; 39(1): 87-99.
  • 80. El Amki M, Wegener S. Improving cerebral blood flow after arterial recanalization: A novel therapeutic strategy in stroke. Int J Mol Sci 2017; 18(12).
  • 81. Espinosa de Rueda M, Parrilla G, Manzano-Fernandez S, et al. Combined multimodal computed tomography score correlates with futile recanalization after thrombectomy in patients with acute stroke. Stroke 2015; 46(9): 2517-2522.
  • 82. Rha JH, Saver JL. The impact of recanalization on ischemic stroke outcome: A meta-analysis. Stroke 2007; 38(3): 967- 973.
  • 83. Kloner RA, King KS, Harrington MG. No-reflow phenomenon in the heart and brain. Am J Physiol Heart Circ Physiol 2018; 315(3): H550-H562.
  • 84. Albers GW, Marks MP, Kemp S, et al. Thrombectomy for stroke at 6 to 16 hours with selection by perfusion imaging. N Engl J Med 2018; 378(8): 708-718.
  • 85. Nogueira RG, Jadhav AP, Haussen DC, et al. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct. N Engl J Med 2018; 378(1): 11-21.
  • 86. Ter Schiphorst A, Charron S, Hassen WB, et al. Tissue no- reflow despite full recanalization following thrombectomy for anterior circulation stroke with proximal occlusion: A clinical study. J Cereb Blood Flow Metab 2021; 41(2): 253- 266.
  • 87. Arsava EM, Arat A, Topcuoglu MA, et al. Angiographic microcirculatory obstructions distal to occlusion signify poor outcome after endovascular treatment for acute ischemic stroke. Transl Stroke Res 2018; 9(1): 44-50.
  • 88. Haitham Hussain AH, Basit Rahim, Adnan Qureshi. Prevalence and effect of 'no reflow' phenomenon following endovascular treatment related recanalization in patients with acute middle cerebral artery occlusion (p07.264). Neurology 2016; 80.
  • 89. Soares BP, Tong E, Hom J, et al. Reperfusion is a more accurate predictor of follow-up infarct volume than recanalization: A proof of concept using ct in acute ischemic stroke patients. Stroke 2010; 41(1): e34-40.
APA Gurler G, Soylu K, Yemisci M (2021). İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. , 179 - 190. 10.5505/tbdhd.2021.83435
Chicago Gurler Gokce,Soylu Kadir Oguzhan,Yemisci Muge İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. (2021): 179 - 190. 10.5505/tbdhd.2021.83435
MLA Gurler Gokce,Soylu Kadir Oguzhan,Yemisci Muge İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. , 2021, ss.179 - 190. 10.5505/tbdhd.2021.83435
AMA Gurler G,Soylu K,Yemisci M İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. . 2021; 179 - 190. 10.5505/tbdhd.2021.83435
Vancouver Gurler G,Soylu K,Yemisci M İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. . 2021; 179 - 190. 10.5505/tbdhd.2021.83435
IEEE Gurler G,Soylu K,Yemisci M "İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW." , ss.179 - 190, 2021. 10.5505/tbdhd.2021.83435
ISNAD Gurler, Gokce vd. "İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW". (2021), 179-190. https://doi.org/10.5505/tbdhd.2021.83435
APA Gurler G, Soylu K, Yemisci M (2021). İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. Türk Beyin Damar Hastalıkları Dergisi, 27(3), 179 - 190. 10.5505/tbdhd.2021.83435
Chicago Gurler Gokce,Soylu Kadir Oguzhan,Yemisci Muge İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. Türk Beyin Damar Hastalıkları Dergisi 27, no.3 (2021): 179 - 190. 10.5505/tbdhd.2021.83435
MLA Gurler Gokce,Soylu Kadir Oguzhan,Yemisci Muge İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. Türk Beyin Damar Hastalıkları Dergisi, vol.27, no.3, 2021, ss.179 - 190. 10.5505/tbdhd.2021.83435
AMA Gurler G,Soylu K,Yemisci M İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. Türk Beyin Damar Hastalıkları Dergisi. 2021; 27(3): 179 - 190. 10.5505/tbdhd.2021.83435
Vancouver Gurler G,Soylu K,Yemisci M İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW. Türk Beyin Damar Hastalıkları Dergisi. 2021; 27(3): 179 - 190. 10.5505/tbdhd.2021.83435
IEEE Gurler G,Soylu K,Yemisci M "İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW." Türk Beyin Damar Hastalıkları Dergisi, 27, ss.179 - 190, 2021. 10.5505/tbdhd.2021.83435
ISNAD Gurler, Gokce vd. "İSKEMİK İNMENİN GİZEMLİ FENOMENİ: NO-REFLOW". Türk Beyin Damar Hastalıkları Dergisi 27/3 (2021), 179-190. https://doi.org/10.5505/tbdhd.2021.83435