TY - JOUR
T1 - Real-time monitoring of endogenous lipid peroxidation by exhaled ethylene in patients undergoing cardiac surgery
AU - Cristescu, Simona M.
AU - Kiss, Rudolf
AU - te Lintel Hekkert, Sacco
AU - Dalby, Miles
AU - Harren, Frans J.M.
AU - Risby, Terence H.
AU - Marczin, Nandor
N1 - Publisher Copyright:
© 2014 the American Physiological Society.
PY - 2014/10/1
Y1 - 2014/10/1
N2 - Pulmonary and systemic organ injury produced by oxidative stress including lipid peroxidation is a fundamental tenet of ischemia-reperfusion injury, inflammatory response to cardiac surgery, and cardiopulmonary bypass (CPB) but is not routinely measured in a surgically relevant time frame. To initiate a paradigm shift toward noninvasive and real-time monitoring of endogenous lipid peroxidation, we have explored pulmonary excretion and dynamism of exhaled breath ethylene during cardiac surgery to test the hypothesis that surgical technique and ischemia-reperfusion triggers lipid peroxidation. We have employed laser photoacoustic spectroscopy to measure real-time trace concentrations of ethylene from the patient breath and from the CPB machine. Patients undergoing aortic or mitral valve surgery-requiring CPB (n = 15) or off-pump coronary artery bypass surgery (OPCAB) (n = 7) were studied. Skin and tissue incision by diathermy caused striking (>30-fold) increases in exhaled ethylene resulting in elevated levels until CPB. Gaseous ethylene in the CPB circuit was raised upon the establishment of CPB (> 10-fold) and decreased over time. Rep-erfusion of myocardium and lungs did not appear to enhance ethylene levels significantly. During OPCAB surgery, we have observed increased ethylene in 16 of 30 documented reperfusion events associated with coronary and aortic anastomoses. Therefore, novel real-time monitoring of endogenous lipid peroxidation in the intraoperative setting provides unparalleled detail of endogenous and surgery-triggered production of ethylene. Diathermy and unprotected regional myocardial ischemia and reperfusion are the most significant contributors to increased ethylene.
AB - Pulmonary and systemic organ injury produced by oxidative stress including lipid peroxidation is a fundamental tenet of ischemia-reperfusion injury, inflammatory response to cardiac surgery, and cardiopulmonary bypass (CPB) but is not routinely measured in a surgically relevant time frame. To initiate a paradigm shift toward noninvasive and real-time monitoring of endogenous lipid peroxidation, we have explored pulmonary excretion and dynamism of exhaled breath ethylene during cardiac surgery to test the hypothesis that surgical technique and ischemia-reperfusion triggers lipid peroxidation. We have employed laser photoacoustic spectroscopy to measure real-time trace concentrations of ethylene from the patient breath and from the CPB machine. Patients undergoing aortic or mitral valve surgery-requiring CPB (n = 15) or off-pump coronary artery bypass surgery (OPCAB) (n = 7) were studied. Skin and tissue incision by diathermy caused striking (>30-fold) increases in exhaled ethylene resulting in elevated levels until CPB. Gaseous ethylene in the CPB circuit was raised upon the establishment of CPB (> 10-fold) and decreased over time. Rep-erfusion of myocardium and lungs did not appear to enhance ethylene levels significantly. During OPCAB surgery, we have observed increased ethylene in 16 of 30 documented reperfusion events associated with coronary and aortic anastomoses. Therefore, novel real-time monitoring of endogenous lipid peroxidation in the intraoperative setting provides unparalleled detail of endogenous and surgery-triggered production of ethylene. Diathermy and unprotected regional myocardial ischemia and reperfusion are the most significant contributors to increased ethylene.
KW - Cardiopulmonary bypass
KW - Ischemia-reperfusion injury
KW - Off-pump coronary artery bypass grafting
KW - Oxidative stress
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U2 - 10.1152/ajplung.00168.2014
DO - 10.1152/ajplung.00168.2014
M3 - Article
C2 - 25128523
AN - SCOPUS:84907542624
SN - 1040-0605
VL - 307
SP - L509-L515
JO - American Journal of Physiology - Lung Cellular and Molecular Physiology
JF - American Journal of Physiology - Lung Cellular and Molecular Physiology
IS - 7
ER -