Abstract

Objective To investigate the effects of Bretschneider’s histidine-tryptophan-ketoglutarate (HTK) solution and cold blood cardioplegia on systemic endothelial functions.Methods A total of 50 patients who underwent isolated coronary artery bypass surgery between March 2018 and May 2018 were randomly divided into two groups - group 1 (Bretschneider’s HTK solution, n=25) and group 2 (cold blood cardioplegia, n=25). Data related to the indicators of endothelial dysfunction were recorded. Flow-mediated dilation was measured together with the assessment of the values of endothelin-1, von Willebrand factor, and asymmetric dimethylarginine to identify endothelial dysfunction. Then, the two groups were compared regarding these values.Results The most significant result of our study was that the endothelin-1 level was significantly higher in group 2 than in group 1 (P<0.001). The value of flow-mediated dilation was found to increase to a lesser degree on the postoperative days compared to the value at the day of admission in group 1 (P=0.002 and P=0.030, respectively).Conclusion Cardiopulmonary bypass leads to endothelial dysfunction. Our results revealed that Bretschneider’s HTK solution causes less severe endothelial injury than cold blood cardioplegia.

Highlights

  • The development of cardiopulmonary bypass (CPB) systems is undoubtedly one of the most significant steps in cardiac surgery

  • The most significant results of our study are that the level of ET-1, which is among the indicators of endothelial dysfunction, has a higher trend, and the flow-mediated dilation (FMD) level is lower in the cold blood cardioplegia (CBC) group when compared to the HTK group

  • Endothelial activation and dysfunction play an important role in morbidity and mortality after CPB as a reason for the development and continuation of systemic inflammation

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Summary

Introduction

The development of cardiopulmonary bypass (CPB) systems is undoubtedly one of the most significant steps in cardiac surgery. Numerous factors, mainly the inflammatory changes due to non-physiological blood flow within nonendothelialized lines, high-dose anticoagulation, together with gas and microparticle emboli, affect the end-organ perfusion adversely during CPB.The two most important causes of mortality following cardiac surgery are incompetent surgical technique and inadequate myocardial protection. Endothelial tissue covering the inner wall of the vessels regulates basic hemostatic functions such as vascular tone, circulation of blood cells, inflammation, and platelet activity by secreted proinflammatory and anti-inflammatory cytokines. All these events, which endothelium maintains in perfect balance, deteriorate when endothelial dysfunction develops, and many pathological conditions occur. It is obvious that CPB disrupts endothelial functions[3]

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