Pathogenesis of ischemia/reperfusion syndrome

Abstract

Ischemia/reperfusion syndrome is a collective concept that combines various pathological conditions developing against the background of the restoration of the main blood flow in the organ or limb segment, which has long been subjected to ischemia or traumatic amputation. Intensive care physicians often see ischemia/reperfusion syndrome after restoration of blood supply in patients with critical ischemia of the lower limb. The rate of critical ischemia of the lower limbs ranges from 400 to 1000 cases per 1 million of the population. The number of lower limb amputations due to critical lower limb ischemia in economically developed countries is 13.7-32.3 cases per 100,000 of the population. The main etiological factors of critical lower limb ischemia are atherosclerosis of peripheral vessels and vascular complications of diabetes. The pathogenesis of ischemia/reperfusion syndrome is based on a complex of pathophysiological changes resulting from the restoration of blood flow in previously ischemic lower limb. Restoration of blood circulation leads to massive flow into the systemic bloodstream of anaerobic metabolism products, free myoglobin, biologically active substances and inflammatory mediators. The main sources of reperfusion damage are activated forms of oxygen, in particular, superoxide radical О2-, nitric oxide, lipid peroxidation products. In the conditions of primary ischemia, and then tissue reperfusion, excessive production of activated oxygen forms leads to damage of biological structures (lipids, proteins, deoxyribonucleic acid), which causes disruption of normal cell functioning or its death due to necrosis or apoptosis, ion pump dysfunction, adhesion of leukocytes and increased vascular permeability.

Keywords

ischemia/reperfusion syndrome / critical lower limb ischemia / activated forms of oxygen / lipid peroxidation / myoglobin

References

[1] Marshalov D.V., Petrenko A.P., Glushach I.A. Reperfusion syndrome: concept, definition, classification. Patologiia krovoobrashcheniia i kardiokhirurgiia. 2008; (3): 67–72. (In Russ.)

[2] Маршалов Д.В., Петренко А.П., Глушач И.А. Реперфузионный синдром: понятие, определение, классификация. Патология кровообращения и кардиохирургия. 2008; (3): 67-72.

[3] Kalinin R.E., Pshennikov A.S., Suchkov I.A. Reperfusion injury of tissues in surgery of arteries of lower extremities. Novosti khirurgii. 2015; 23 (3): 348–352. (In Russ.)

[4] Калинин Р.Е., Пшенников А.С., Сучков И.А. Реперфузионное повреждение тканей в хирургии артерий нижних конечностей. Новости хирургии. 2015; 23 (3): 348-352. DOI: 10.18484/2305-0047.2015.3.348.

[5] Zasimovich V.N., Ioskevich N.N. Reperfusion (reoxygenation) injury as a problem of the artery reconstructive surgery in atherosclerotic genesis chronic ischemia of the lower limbs. Novosti khirurgii. 2017; 25 (6): 632–642. (In Russ.)

[6] Засимович В.Н., Иоскевич Н.Н. Реперфузионно-реоксигенационный синдром как проблема реконструктивной хирургии артерий при хронической ишемии нижних конечностей атеросклеротического генеза. Новости хирургии. 2017; 26 (6): 632-642. DOI: 10.18484/2305-0047.2017.6.632.

[7] Gavrilenko A.V., Kotov A.E., Ul’yanov N.D. Predicting the results of surgical treatment of the critical lower limb ischemia. Khirurgiya. 2013; (5): 68–72. (In Russ.)

[8] Гавриленко А.В., Котов А.Э., Ульянов Н.Д. Прогнозирование результатов хирургического лечения больных с критической ишемией нижних конечностей методами оценки регионарного кровотока. Хирургия. 2013; (5): 68-72.

[9] Norgren L., Hiat W.R., Dormandy J.A. et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J. Vasc. Endovasc. Surg. 2007; 33: 1–75. DOI: 10.1016/j.ejvs.2006.09.024.

[10] Norgren L., Hiat W.R., Dormandy J.A. et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J. Vasc. Endovasc. Surg. 2007; 33: 1-75. DOI: 10.1016/j.ejvs.2006.09.024.

[11] Zudin A.M., Zasorina M.A., Orlova M.A. Epidemiology of chronic critical limb ischemia. Khirurgiya. 2014; (10): 91–95. (In Russ.)

[12] Зудин А.М., Засорина М.А., Орлова М.А. Эпидемиологические аспекты хронической критической ишемии нижних конечностей. Хирургия. 2014; (10): 91-95.

[13] Pasechnik I.N., Skobelev E.I., Krylov V.V. et al. Abdominal sepsis and oxidative stress. Khirurgiya. 2015; (12): 18–23. (In Russ.)

[14] Пасечник И.Н., Скобелев Е.И., Крылов В.В. и др. Абдоминальный сепсис и окислительный стресс. Хирургия. 2015; (12): 18-23. DOI: 10.17116/hirugia20151218-23.

[15] Klinicheskie rekomendatsii po vedeniyu patsientov s sosudistoy arterial’noy patologiey (Rossiyskiy soglasitel’nyy dokument). Chast’ 1. Perifericheskie arterii. (Clinical recommendations on management of patients with vascular arterial pathology (Russian conciliation document). Part 1. Peripheral arteries.) Ed. by L.A. Bokeriya. Moscow: Pub. NTsSSKh A.N. Bakuleva RAMS. 2010; 176 p. (In Russ.)

[16] Клинические рекомендации по ведению пациентов с сосудистой артериальной патологией (Российский согласительный документ). Часть 1. Периферические артерии. Под ред. Л.А. Бокерия. М.: Изд-во НЦССХ им. А.Н. Бакулева РАМН. 2010; 176 c.

[17] Becker F., Robert-Ebadi H., Ricco J.B. et al. Chapter I. Definitions, epidemiology, clinical presentation and prognosis. Eur. J. Vasc. Endovasc. Surg. 2011; 42 (2): 4–12. DOI: 10.1016/s1078-5884(11)60009-9.

[18] Becker F., Robert-Ebadi H., Ricco J.B. et al. Chapter I. Definitions, epidemiology, clinical presentation and prognosis. Eur. J. Vasc. Endovasc. Surg. 2011; 42 (2): 4-12. DOI: 10.1016/s1078-5884(11)60009-9.

[19] Pasechnik I.N. Oxidative stress and critical conditions in surgical patients. Vestnik intensivnoy terapii. 2004; (3): 27–31. (In Russ.)

[20] Пасечник И.Н. Окислительный стресс и критические состояния у хирургических больных. Вестн. интенсив. терап. 2004; (3): 27-31.

[21] Caccese D., Pratico D., Ghiselli A. et al. Superoxide anion and hydroxyl radical release by collagen-induced platelet aggregation — role of arachidonic acid metabolism. Thromb. Haemost. 2000; 83: 485–490. DOI: 1001046464.

[22] Caccese D., Pratico D., Ghiselli A. et al. Superoxide anion and hydroxyl radical release by collagen-induced platelet aggregation - role of arachidonic acid metabolism. Thromb. Haemost. 2000; 83: 485-490. DOI: 1001046464.

[23] Yates С.М., Abdelhamid М., Adam D.J. et al. Endovascular aneurysm repair reverses the increased titer and the inflammatory activity of interleukin-1alpha in the serum of patients with abdominal aortic aneurysm. J. Vasc. Surg. 2011; 54 (2): 497–503. DOI: 10.1016/j.jvs.2011.02.054.

[24] Yates С.М., Abdelhamid М., Adam D.J. et al. Endovascular aneurysm repair reverses the increased titer and the inflammatory activity of interleukin-1alpha in the serum of patients with abdominal aortic aneurysm. J. Vasc. Surg. 2011; 54 (2): 497-503. DOI: 10.1016/j.jvs.2011.02.054.

[25] Pasechnik I.N., Meshcheryakov A.A., Sychev A.V. Efficacy of oxidative stress treatment in surgical patients with acute abdominal diseases in perioperative period. Rossiyskie meditsinskie vesti. 2009; 14 (3): 50–55. (In Russ.)

[26] Пасечник И.Н., Мещеряков А.А., Сычёв А.В. Эффективность коррекции окислительного стресса у хирургических больных с острой абдоминальной патологией в периоперационном периоде. Рос. мед. вести. 2009; 14 (3): 50-55.

[27] Koksal G.M. Oxidative stress and its complications in human health. Advanc. Biosci. Biotechnol. 2012; 3 (8): 1113–1115. DOI: 10.4236/abb.2012.38136.

[28] Koksal G.M. Oxidative stress and its complications in human health. Advanc. Biosci. Biotechnol. 2012; 3 (8): 1113-1115. DOI: 10.4236/abb.2012.38136.

[29] Rodrigues S.F., Granger D.N. Role of blood cells in ischemia-reperfusion-induced endothelial barrier failure. Cardiovasc. Res. 2010; 87 (2): 291–299. DOI: 10.1093/cvr/cvq090.

[30] Rodrigues S.F., Granger D.N. Role of blood cells in ischemia-reperfusion-induced endothelial barrier failure. Cardiovasc. Res. 2010; 87 (2): 291-299. DOI: 10.1093/cvr/cvq090.

[31] Gladwin M.T., Kato G.J., Weiner D. et al. Nitric oxide for inhalation in the acute treatment of sickle cell pain crisis: a randomized controlled trial. JAMA. 2011; 305 (9): 893–902. DOI: 0.1001/jama.2011.235.

[32] Gladwin M.T., Kato G.J., Weiner D. et al. Nitric oxide for inhalation in the acute treatment of sickle cell pain crisis: a randomized controlled trial. JAMA. 2011; 305 (9): 893-902. DOI: 0.1001/jama.2011.235.

[33] Carr A.C., van den Berg J.J., Winterbourn C.C. Chlorination of cholesterol in cell membranes by hypochlous acid. Arch. Biochem. Biophys. 1996; 332: 63–69. DOI: 10/1006/abbi.1996.0317.

[34] Carr A.C., van den Berg J.J., Winterbourn C.C. Chlorination of cholesterol in cell membranes by hypochlous acid. Arch. Biochem. Biophys. 1996; 332: 63-69. DOI: 10/1006/abbi.1996.0317.

[35] Smirnov A.V., Dobronravov V.A., Rumyantsev A.Sh., Kayukov I.G. Ostroe povrezhdenie pochek. (Acute kidney injury.) Moscow: MIA. 2015; 488 p. (In Russ.)

[36] Смирнов А.В., Добронравов В.А., Румянцев А.Ш., Каюков И.Г. Острое повреждение почек. М.: МИА. 2015; 488 c.

[37] Baines C.P. How and when do myocytes die during ischemia and reperfusion: the late phase. J. Cardiovasc. Pharmacol. Ther. 2011; 16 (3–4): 239–243. DOI: 10.1177/1074248411407769.

[38] Baines C.P. How and when do myocytes die during ischemia and reperfusion: the late phase. J. Cardiovasc. Pharmacol. Ther. 2011; 16 (3-4): 239-243. DOI: 10.1177/1074248411407769.

[39] Semenov V.N., Pasechnik I.N. Apoptosis and its role in the pathogenesis of critical states. Vestnik intensivnoy terapii. 2004; (1): 3–7. (In Russ.)

[40] Семёнов В.Н., Пасечник И.Н. Апоптоз и его роль в патогенезе критических состояний. Вестн. интенсив. терап. 2004; (1): 3-7.

[41] Hancock J.T., Desikan R., Neill S.J. Role of reactive oxygen species in cell signaling pathways. Biochem. Soc. Trans. 2001; 29: 345–350. DOI: 10.1042/bst0290345.

[42] Hancock J.T., Desikan R., Neill S.J. Role of reactive oxygen species in cell signaling pathways. Biochem. Soc. Trans. 2001; 29: 345-350. DOI: 10.1042/bst0290345.

RIGHTS & PERMISSIONS

Kutepov D.E., Zhigalova M.S., Pasechnik I.N.