Severe Acute Pancreatitis: A Possible Role of Intramyocardial Cytokine Production

  • Alberto Meyer Department of Gastroenterology (LIM-37), School of Medicine, University of São Paulo, São Paulo, Brazil
  • Márcia S Kubrusly Department of Gastroenterology (LIM-37), School of Medicine, University of São Paulo, São Paulo, Brazil
  • Vera M Salemi Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo, Brazil
  • Ana M de Mendonça Coelho Department of Gastroenterology (LIM-37), School of Medicine, University of São Paulo, São Paulo, Brazil
  • Nilza A T Molan Department of Gastroenterology (LIM-37), School of Medicine, University of São Paulo, São Paulo, Brazil
  • Roseli A Patzina Department of Pathology, School of Medicine, University of São Paulo, São Paulo, Brazil
  • Marcel C C Machado Emergency Medicine Department, School of Medicine, University of São Paulo, São Paulo, Brazil
  • Charles Mady Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo, Brazil
  • Luiz A C D’Albuquerque Department of Gastroenterology (LIM-37), School of Medicine, University of São Paulo, São Paulo, Brazil
  • José Jukemura Department of Gastroenterology (LIM-37), School of Medicine, University of São Paulo, São Paulo, Brazil
Keywords: Cytokines, Heart/ physiopathology, Pancreatitis/ physiopathology

Abstract

Context Several mechanisms are involved in the development of the local and systemic response in acute pancreatitis. Cardiovascular system may be affected throughout the clinical course of acute pancreatitis. The aim was to evaluate local myocardial cytokine production, as well as, functional and histological myocardial alterations in severe acute pancreatitis. Methods The animals were divided into three groups: Group 1: control; Group 2: sham; Group 3: severe acute pancreatitis. Echocardiographic assessment of cardiac function, serum levels of amylase and cytokines (TNF-α, IL-6 and IL-10), and mRNA expression of TNF-α, IL-6 and TGF-β were measured. Myocardial tissue alterations were analysed by histological examination. Results The serum TNF-α and IL-10 levels were significant higher in AP 2h group. The mRNA IL-6 levels from group AP 2h were statistically higher. The mRNA TNF-α level from sham group and AP 2h were statistically lower. Significant changes in the left ventricular diameter were found in AP 2h and AP 12h groups. There were statistical changes for vacuolar degeneration, picnosis and loss of nucleus, and lymphocytes. Conclusion We found cardiac and histological changes compatible with the inflammatory process triggered by SAP with the promotion of local myocardial cytokine production.

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References

Talukdar R, SwaroopVege S. Early management of severe acute pancreatitis. Curr Gastroenterol Rep. 2011; 13(2):123-30. [PMID:

Wu BU. Prognosis in acute pancreatitis. CMAJ. 2011; 183(6):673-7. [PMID: 21422134]

Makhija R, Kingsnorth AN. Cytokine storm in acute pancreatitis. J Hepatobiliary Pancreat Surg. 2002; 9:401-10. [PMID: 12483260]

Norman J. The role of cytokines in the pathogenesis of acute pancreatitis. Am J Surg. 1998; 175(1):76-83. [PMID: 9445247]

Campos T, Deree J, Coimbra R. From acute pancreatitis to end-organ injury: mechanisms of acute lung injury. Surg Infect. 2007; 8(1):107-20. [PMID: 17381402]

Yegneswaran B, Kostis JB, Pitchumoni CS. Cardiovascular manifestations of acute pancreatitis. J Crit Care. 2011; 26(2):225. [PMID: 21185146]

Greer SE, BurchardK W. Acute pancreatitis and critical illness: a pancreatic tale of hypoperfusion and inflammation. Chest. 2009;

(5):1413-9. [PMID: 19892682]

Kanaian AS, Permiakov NK, Khandanian RK, Gevorkian GA. Combined pathology of the pancreas and myocardium in myocardial infarction and acute destructive pancreatitis. Arkh Patol. 1996; 58(5):56-61. [PMID: 9005827]

Saulea A, Costin S, Rotari V. Heart ultrastructure in experimental acute pancreatitis. Rom J Physiol. 1997; 34(1-4):35-44. [PMID: 9653808]

Lankisch PG, Koop H, Winckler K, Fölsch UR, Creutzfeldt W. Somatostatin therapy of acute experimental pancreatitis. Gut. 1977; 18(9):713-6. [PMID: 604191]

Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2 (-Delta Delta C(T)) method. Methods. 2001; 25:402-8. [PMID: 11846609]

Salemi VM, Pires MD, Cestari IN, Cestari IA, Picard MH, Leirner AA et al. Echocardiographic assessment of global ventricular function using the myocardial performance index in rats with hypertrophy. Artif Organs. 2004; 28:332-7. [PMID: 15084191]

Granger J, Remick D. Acute pancreatitis: models, markers and mediators. Shock. 2005; 24:45-51. [PMID: 16374372]

Steptoe A, Hamer M, Chida Y. The effects of acute psychological stress on circulating inflammatory factors in humans: a review and meta- analysis. Brain Behav Immun. 2007; 21(7):901-12. [PMID: 17475444]

Dumot JA, Conwell DL, Zuccaro G Jr, Vargo JJ, Shay SS, Easley KA et al. A randomized, double blind study of interleukin 10 for the prevention of ERCP-induced pancreatitis. Am J Gastroenterol. 2001; 96(7):2098-102. [PMID: 11467638]

Di Carlo V, Nespoli A, Chiesa R, Staudacher C, Cristallo M, Bevilacqua G et al. Hemodynamic and metabolic impairment in acute pancreatitis. World J Surg. 1981; 5(3):329-39. [PMID: 7293195]

Ito K, Ramirez-Schon G, Shah PM, Agarwal N, Delguercio LR, Reynolds BM. Myocardial function in acute pancreatitis. Ann Surg. 1981; 194:85-8. [PMID: 7247538]

Burrell LM, Chan R, Phillips PA, Calafiore P, Tonkin AM, Johnston CI. Validation of an echocardiographic assessment of cardiac function following moderate size myocardial infarction in the rat. Clin Exp Pharmacol Physiol. 1996; 23(6-7):570-2. [PMID: 8800587]

Ridker PM, Rifai N, Stampfer MJ, Hennekens CH. Plasma concentration of interleukin-6 and the risk of future myocardial infarction among apparently healthy men. Circulation. 2000; 101:1767–72. [PMID: 10769275]

Danesh J, Kaptoge S, Mann AG, Sarwar N, Wood A, Angleman SB et al. Long-term interleukin-6 levels and subsequent risk of coronary heart disease: two new prospective studies and a systematic review. PLoS Med. 2008; 5(4):78. [PMID: 18399716]

Flierl MA, Rittirsch D, Huber-Lang MS, Sarma JV, Ward PA. Molecular events in the cardiomyopathy of sepsis. Mol Med. 2008; 14(5-6):327-36. [PMID: 18256728]

Flynn A, Chokkalingam Mani B, Mather PJ. Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms. Heart Fail Rev. 2010; 15(6):605-11. [PMID: 20571889]

Flores-Arredondo JH, García-Rivas G, Torre-Amione G. Immune Modulation in Heart Failure: Past Challenges and Future Hopes. Curr Heart Fail Rep. 2011; 8:28-37. [PMID: 21221862]

Zhang C, Jin S, Guo W, Li C, Li X, Rane MJ et al. Attenuation of diabetes- induced cardiac inflammation and pathological remodeling by low-dose radiation. Radiat Res. 2011; 175(3):307-21. [PMID: 21388274]

Plenz G, Eschert H, Erren M, Wichter T, Böhm M, Flesch M et al. The interleukin-6/interleukin-6-receptor system is activated in donor hearts. J Am Coll Cardiol. 2002; 39(9):1508-12. [PMID: 11985915]

Kai H, Kuwahara F, Tokuda K, Imaizumi T. Diastolic dysfunction in hypertensive hearts: roles of perivascular inflammation and reactive myocardial fibrosis. Hypertens Res. 2005; 28(6):483-90. [PMID: 16231753]

Kuwahara F, Kai H, Tokuda K, Kai M, Takeshita A, Egashira K et al. Transforming growth factor-beta function blocking prevents myocardial fibrosis and diastolic dysfunction in pressure-overloaded rats. Circulation. 2002; 106(1):130-5. [PMID: 12093782]

Ridker PM, Rifai N, Pfeffer M, Sacks F, Lepage S, Braunwald E. Elevation of tumor necrosis factor-alpha and increased risk of recurrent coronary events after myocardial infarction. Circulation. 2000; 101(18):2149-53. [PMID: 10801754]

Solomon MA, Correa R, Alexander HR, Koev LA, Cobb JP, Kim DK et al. Myocardial energy metabolism and morphology in a canine model of sepsis. Am J Physiol. 1994; 266(2):757-68. [PMID: 8141377]

Zhou M, Wang P, Chaudry IH. Cardiac contractility and structure are not significantly compromised even during the late, hypodynamic stage of sepsis. Shock. 1998; 9(5):352-8. [PMID: 9617885]

Rossi MA, Celes MR, Prado CM, Saggioro FP. Myocardial structural changes in long-term human severe sepsis/septic shock may be responsible for cardiac dysfunction. Shock. 2007; 27(1):10-8. [PMID: 17172974]

Azzawi M, Kan SW, Hillier V, Yonan N, Hutchinson IV, Hasleton PS. The distribution of cardiac macrophages in myocardial ischaemia and cardiomyopathy. Histopathology. 2005; 46(3):314-9. [PMID: 15720417]

Boxplot of LVEDD
Published
2014-05-27
How to Cite
Meyer, A., Kubrusly, M., Salemi, V., de Mendonça Coelho, A., Molan, N., Patzina, R., Machado, M., Mady, C., D’Albuquerque, L., & Jukemura, J. (2014). Severe Acute Pancreatitis: A Possible Role of Intramyocardial Cytokine Production. JOP. Journal of the Pancreas, 15(3), 237-242. https://doi.org/10.6092/1590-8577/2171
Section
ORIGINAL ARTICLES