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Thiol/disulfide homeostasis in pericardial fluid and plasma of patients undergoing coronary artery bypass surgery
  • Reşat Dikme,
  • Abdullah Taşkın
Reşat Dikme
Harran Universitesi

Corresponding Author:rdikme@harran.edu.tr

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Abdullah Taşkın
Harran Universitesi - Osmanbey Kampusu
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Abstract

Background: On-pump coronary artery bypass grafting (CABG) method affect almost all biochemical reactions by disrupting the patient’s redox homeostasis. Detection of systemic redox hemostasis in the patient are critical for the CABG method’s success and the prognosis of the disease. In this study, thiol/disulfide parameters, which are indicators of redox homeostasis, and ischemia-modified albumin (IMA) levels in the plasma and pericardial fluid of patients who underwent coronary artery bypass surgery were investigated. Methods: Sixty patients who underwent an on-pump CABG operation with the Cardiopulmonary Bypass (CPB) method were included in this study. Blood samples were taken from the patients before and after the CPB. Pericardial fluid samples were taken before the CPB. Then, thiol/disulfide homeostasis, albümin, and IMA levels in the pericardial fluid, and the patients’ plasma levels were compared. Results: Albumin and IMA levels were significantly higher in postop compared to preop (p < 0.001). Thiol/disulfide parameters, native thiol, total thiol, and disulfide levels were higher and statistically significant in preop than in postoperative examinations (p < 0.001). A negative correlation was found between pericardial fluid IMA and thiol-disulfide parameters (p < 0.001). Conclusions: Changes in thiol/disulfide homeostasis, albümin, and IMA levels at different times during the on-pump CABG may be caused by foreign non-endothelial surfaces, filters, the reperfusion process, and pharmacological effects in the extracorporeal circulation. Thiol/disulfide homeostasis, albumin, and IMA levels should be monitored during the on-pump CABG and should intervene with appropriate therapeutic strategies. In this way, secondary pathologies can be avoided by preventing cellular damage and excessive inflammatory responses.