NDLI: Myocardial preconditioning reduces kidney injury and apoptosis induced by myocardial ischaemia and reperfusion.

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Myocardial preconditioning reduces kidney injury and apoptosis induced by myocardial ischaemia and reperfusion.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Huang, Cheng-Hsiung Lai, Chang-Chi Yang, An-Han Chiang, Shu-Chiung
Description	Country affiliation: Taiwan Author Affiliation: Huang CH ( Division of Cardiovascular Surgery, Department of Surgery, National Yang-Ming University School of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan chhuang@vghtpe.gov.tw.); Lai CC ( Institute of Clinical Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan.); Yang AH ( Department of Pathology and Laboratory Medicine, National Yang-Ming University School of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.); Chiang SC ( Institute of Hospital and Health Care Administration, National Yang-Ming University School of Medicine, Taipei, Taiwan.)
Abstract	OBJECTIVES: Acute kidney injury is a common and serious complication of cardiac surgery. Because its underlying mechanisms are unclear, there is no specific therapy to prevent or treat it. A regional transient ischaemia and reperfusion (I/R) may provide protection to distant tissue or organs, a phenomenon known as remote preconditioning. In this study, we investigated whether myocardial preconditioning (MPC) would reduce kidney injury and apoptosis induced by myocardial I/R, as well as the mechanisms involved. METHODS: Myocardial I/R was induced by a 40-min occlusion of the left anterior descending artery and a 3-h reperfusion in anaesthetized Sprague-Dawley rats. MPC was elicited by two 10-min coronary artery occlusions and two 10-min reperfusions. A sham group received the same surgical procedures without coronary artery occlusion and reperfusion. RESULTS: Compared with the sham group, myocardial I/R significantly increased the serum creatinine levels (1.15 ± 0.44 vs 0.54 ± 0.23 mg/dl, P < 0.05, mean ± standard deviation) and renal histological damage, indicating increased kidney injury. Kidney apoptosis was also significantly increased, as evidenced by the increase in the terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate (dUTP) nick-end labelling (TUNEL)-positive nuclei, clear DNA laddering and increased caspase-3 activation. Serum levels of tumour necrosis factor- (TNF- ), interleukin-1 (IL-1) and interleukin-6 (IL-6) were significantly elevated, as were TNF- levels in the kidneys. MPC significantly decreased myocardial infarct size (18.5 ± 3.1 vs 25.6 ± 2.1% of area at risk, P < 0.001). Additionally, MPC significantly reduced the serum creatinine level (0.65 ± 0.19 mg/dl, P < 0.05), renal histological damage and apoptosis. The increase in the serum levels of TNF- , IL-1 and IL-6, and of TNF- in the kidneys, was significantly inhibited. Western blot analysis found that MPC significantly increased Bcl-2 and decreased Bax in the kidneys. Phosphorylation of Akt and extracellular signal-regulated kinases 1 and 2 (ERK1/2) was significantly increased. Haemodynamics, area at risk and mortality did not differ significantly among the groups. CONCLUSIONS: MPC significantly reduces kidney injury and apoptosis induced by myocardial I/R. The underlying mechanisms might be related to inhibition of both the extrinsic and intrinsic pathways of apoptosis, possibly via inhibition of TNF- production, modulation of Bcl-2 and Bax and activation of Akt and ERK1/2.
File Format	HTM / HTML
ISSN	10107940
e-ISSN	1873734X
Journal	European Journal of Cardio-Thoracic Surgery
Issue Number	3
Volume Number	48
Language	English
Publisher	Oxford University Press
Publisher Date	2015-09-01
Publisher Place	Germany
Access Restriction	Open
Subject Keyword	Discipline Cardiology__semicolon__surgery Acute Kidney Injury Prevention & Control Apoptosis Physiology Ischemic Preconditioning, Myocardial Myocardial Ischemia Complications Myocardial Reperfusion Injury Pathology Animals Caspase 3 Interleukin-1 Blood Interleukin-6 Kidney Chemistry Proto-oncogene Proteins C-akt Proto-oncogene Proteins C-bcl-2 Rats, Sprague-dawley Tumor Necrosis Factor-alpha Bcl-2-associated X Protein Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Pulmonary and Respiratory Medicine Surgery Cardiology and Cardiovascular Medicine

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