Clinical Physiology of Circulation

Chief Editor

Leo A. Bockeria, MD, PhD, DSc, Professor, Academician of Russian Academy of Sciences, President of Bakoulev National Medical Research Center for Cardiovascular Surgery


Aspects of mods pathogenesis in cardiac surgery patients

Authors: M .M . Rybka

Company:
A.N. Bakoulev Scientific Center for Cardiovascular Surgery, Ministry of Health of the Russia, Rublevskoe shosse, 135, Moscow, 121552, Russian Federation

E-mail: Сведения доступны для зарегистрированных пользователей.

UDC: 616-083.98:616.12/14-089.168

Link: Clinical Physiology of Blood Circulaiton. 2016; 13 (2): 65-74

Quote as: Rybka M.M. Aspects of mods pathogenesis in cardiac surgery patients. Klinicheskaya Fiziologiya Krovoobrashcheniya (Clinical Physiology of Circulation, Russian journal). 2016; 13 (2): 65-74 (in Russ.)

Received / Accepted:  06.05.2016/11.05.2016

Download
Full text:  

Abstract

As is customary a literature on the pathogenesis of MODS focuses on the biochemical and cytological mechanisms of systemic inflammatory syndrome. This review focuses on the processes of ischemic and reperfusion damage of cells and tissues as the fundamental reason for the development of organ dysfunction and multiple organ failure. It is shown that microcirculation disorders are the cause of disorders of oxygen delivery to cells. At the same time the capillaries themselves undergo ischemia and reperfusion injury. Drastic changes in blood volume, minute flow rate typical of cardiac surgery are the factors leading to dysfunction of microcirculation, disturbance of oxygen delivery and the development of the IRI in cardiac surgical patients.

References

1. WarrenO.J., SmithAJ., AlexiouC., RogersP.L., JawadN., Vincent C. et al. The inflammatory response to cardio­pulmonary bypass: part 1 — mechanisms of pathogene­sis. J. Cardiothorac. Vase. Anesth. 2009; 23 (2): 223—31.

2. Pintar T., Collard C.D. The systemic inflammatory response to cardiopulmonary bypass. Anesthesiol. Clin. North. America. 2003; 21 (3): 453—64.

3. McITwain R.B., Timpa J.G., Kurundkar A.R., Holt D.W., Kelly D.R., Hartman Y.E. et al. Plasma concentrations of inflammatory cytokines rise rapidly during ECMO- related SIRS due to the release of preformed stores in the intestine. Lab. Invest. 2010; 90 (1): 128—39.

4. Бабаев M.A. Синдром полиорганной недостаточ­ности после сердечно-сосудистых операций в усло­виях искусственного кровообращения. Дис. ... д-ра мед. наук. М.; 2011.

5. Лобачева ЕВ. Факторы риска развития ранних ос­ложнений и их коррекция у больных после опера­ций на открытом сердце. Автореф. дис. ... д-ра мед. наук. М.; 2000: 12—44.

6. Еребенчиков О.А., Лихванцев В.В., Плотников Е.Ю., Силачев Д.Н., Певзнер И.Б., Зорова Л.Д., Зоров Д.Б. Молекулярные механизмы развития и адресная терапия синдрома ишемии-реперфузии. Анесте­зиология и реаниматология. 2014; 3: 59—67.

7. Neary R, Redmond Н.Р. Ischaemia/reperfusion injury and the systemic inflammatory response syndrome. In: Grace RA., Mathie R.T (eds). Ischemia-Reperfusion Injury. London: Blackwell Science: 1999; 123—36.

8. Davies M.G., Juynh T.T.T., Hagen P.-О. Endothelial physiology. In: Grace RA., Mathie R.T. (eds). Ischemia-Reperfusion Injury. London: Blackwell Science: 1999; 157-79.

9. Kalogeris T, Baines C.R, Krenz M., Korthuis R.J. Cell biology of ischemia/reperfusion injury. International Review of Cell and Molecular Biology. 2012; 298: 229-317.

10. Moens A.L., Champion H.C., Claeys M.J., Tavazzi B., Kaminski EM., Wolin M.S. et al. High-dose folic acid pretreatment blunts cardiac dysfunction during ischemia coupled to maintenance of high-energy phos­phates and reduces postreperfusion injury. Circulation. 2008; 117: 1810-9.

11. Slone E.A., Fleming S.D. Membrane lipid interactions in intestinal ischemia/reperfusion-induced Injury. Clin. Immunol. 2014; 153 (1): 228-40.

12. Kvietys P.R., Granger D.N. Endothelial cell monolayers as a tool for studying microvascular pathophysiology. Am. I. Physiol. 1997; 273: G1189-G1199.

13. Schofield Z.V., Woodruff T.M., Halai R., Wu M.C., Cooper M.A. Neutrophils-a key component of ischemia- reperfusion injury. Shock, 2013; 40 (6): 463—70.

14. Harrison D.G. Cellular and molecular mechanisms of endothelial cell dysfunction. I. Clin. Invest. 1997; 100: 2153-7.

15. Harris N.R. Opposing effects of L-NAME on capillary filtration rate in the presence or absence of neutrophils. Am. I. Physiol. 1997; 273: G1320-G1325.

16. EppihimerMJ., Russell J., Anderson D.C., Epstein C.J., Laroux S., Granger D.N. Modulation of P-selectin expression in the postischemic intestinal microvascula­ture. Am. /. Physiol. 1997; 273: G1326-G1332.

17. Ichikawa H., Flores S., Kvietys ER. et al. Molecular mechanisms of anoxia/reoxygenation-induced neu­trophil adherence to cultured endothelial cells. Circ. Res. 1997; 81: 922-31.

18. Panes J., Perry M., Granger D.N. Leukocyte endothe­lial cell adhesion: Avenues for therapeutic intervention. Br. J. Pharmacol. 1999; 126: 537—50.

19. Carden D.L., Granger D.N. Pathophysiology of ischaemia - reperfusion injury. I. Pathol. 2000; 190: 255—66.

20. Rao Jianhuaa, Lu Linga, Zhai Yuana. T cells in organ ischemia reperfusion injury. Curr. Opin. Organ. Transplant. 2014; 19 (2): 115—20.

21. Collard C.D., Gelman S. Pathophysiology, clinical manifestations, and prevention of ischemia-reperfusion injury. Anesthesiology. 2001; 94: 1133—8.

22. Granger D.N. Ischemia-reperfusion: mechanisms of microvascular dysfunction and the influence of risk fac­tors for cardiovascular disease. Microcirculation. 1999; 6: 167-78.

23. Galasso G., Schiekofer S., D'Anna C., Gioia G.D., Piccolo R., Niglio T et al. No-reflow phenomenon: pathophysiology, diagnosis, prevention, and treatment. A review of the current literature and future perspec­tives. Angiology. 2014; 65 (3): 180—9.

24. Romson J.L., Hook B.G., Kunkel S.L., Abrams G.D., Schork M.A., Lucchesi B.R. Reduction of the extent of ischemic myocardial injury by neutrophil depletion in the dog. Circulation. 1983; 67: 1016—23.

25. Lee H.L., Chen C.L., Yeh S.T., Zweier J.L., Chen YR. Biphasic modulation of the mitochondrial electron transport chain in myocardial ischemia and reperfusion. Am. J. Physiol. 2012; 302: H1410-H1422.

26. Kalogeris T., Bao Y, Korthuis R.J. Mitochondrial reac­tive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning. Redox Biol. 2014; 2: 702-14.

27. Andreadou I., Iliodromitis E.K., Farmakis D., Kremastinos D.T To prevent, protect and save the ischemic heart: antioxidants revisited. Expert Opinion on Therapeutic Targets. 2009; 13: 945—56.

28. Neuhof C., Neuhof H. Calpain system and its involve­ment in myocardial ischemia and reperfusion injury. World J. Cardiol. 2014; 6 (7): 638-52.

29. Tano J.Y., Gollasch M. Calcium-activated potassium channels in ischemia reperfusion: a brief update. Front Physiol. 2014; 5: 381.

30. Moran J.L., Chalwin R.P., Graham PL. Extracorporeal membrane oxygenation (ECMO) reconsidered. Crit. Care Resusc. 2010; 12 (2): 131—5.

31. Calo L., Dong Y, Kumar R., Przyklenk K., Sander­son TH. Mitochondrial dynamics: an emerging para­digm in ischemia-reperfusion injury. Curr. Pharm. Des. 2013; 19 (39): 6848-57.

32. Даценко C.B., Баутин A.E., Ташханов Д.М. и др. Кардиопротективный эффект дистантного ишеми­ческого прекондиционирования у пациентов, пе­ренесших протезирование аортального клапана. Регионарное кровообращение и микроциркуляция. 2014; 13(1): С35-41.

33. Pac-Soo С.К., Mathew Н., Ма D. Ischaemic condition­ing strategies reduce ischaemia/reperfusion-induced organ injury. Br. J. Anaesth. 2015; 114 (2): 204—16.

34. Alvarez R, Tapia L., Mardones L.A., Pedemonte J.C., Farias J.G., Castillo R.L. Cellular mechanisms against ischemia reperfusion injury induced by the use of anes­thetic pharmacological agents. Chem. Biol. Interact. 2014; 218: 89-98.

35. Le Page S., Prunier F. Remote ischemic conditioning: Current clinical perspectives. J. Cardiol. 2015; 66 (2): 91-6.

36. Vega V.L., Mardones L., Maldonado M., Nicovani S., Manriquez V, Roa J., Ward PH. Xanthine oxidase released from reperfused hind limbs mediate kupffer cell activation, neutrophil sequestration, and hepatic oxidative stress in rats subjected to tourniquet shock. Shock. 2000; 14 (5): 565-71.

37. He B., Xiao J., RenAJ., Zhang YF., Zhang H., ChenM. et al. Role of miR-1 and miR-133a in myocardial
ischemic postconditioning. J. Biomed. Sci. 2011; 18 (1): 1-10.

38. XuX., KriegelAJ., JiaoX., LiuH., BaiX., OlsonJ. etal. miR-21 in ischemia/reperfusion injury: a double-edged sword? Physiol. Genomics. 2014; 46 (21): 789—97.

39. Jaxa-Chamiec T, Bednarz B., Herbaczynska-Cedro K., Maciejewski R, Ceremuzynski L. Effects of vitamins C and E on the outcome after acute myocardial infarction in diabetics: aretrospective, hypothesis-generating analysis from the MIVIT study. Cardiology. 2009; 112: 219-23.

40. Duehrkop C., Rieben R. Ischemia/reperfusion injury: effect of simultaneous inhibition of plasma cascade sys­tems versus specific complement inhibition. Biochem. Pharmacol. 2014; 88 (1): 12—22.

41. Landoni G., Greco T, Biondi-Zoccai G., Nigro Neto C., Febres D., Pintaudi M. et al. Anaesthetic drugs and sur­vival: a Bayesian network meta-analysis of randomized trials in cardiac surgery. Br. J. Anaesth. 2013; 111: 886-96.

42. Zangrillo A., Testa V., Aldrovandi V., Tuoro A., Casirag- hi G., Cavenago F. et al. Volatile agents for cardiac pro­tection in noncardiac surgery: a randomized controlled study. J. Cardiothorac. Vase. Anesth. 2011; 25: 902—7.

43. Lurati Buse G.A., Schumacher R, Seeberger E., Studer W., Schuman R.M., Fassl J. et al. Randomized comparison of sevoflurane vs. propofol to reduce peri­operative myocardial ischemia in patients undergoing noncardiac surgery. Circulation. 2012; 126: 2696—704.

About Authors

Rybka Mikhail Mikhailovich, MD, PhD, Chief of Department of Anaesthesiology and Resuscitation

 If you found mistakes, select text and press Alt+A