19 January 2018 Optical metabolic imaging of irradiated rat heart exposed to ischemia–reperfusion injury
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Abstract
Whole thoracic irradiation (WTI) is known to cause deterioration in cardiac function. Whether irradiation predisposes the heart to further ischemia and reperfusion (IR) injury is not well known. The aim of this study is to examine the susceptibility of rat hearts to IR injury following a single fraction of 15 Gy WTI and to investigate the role of mitochondrial metabolism in the differential susceptibility to IR injury. After day 35 of irradiation, ex vivo hearts from irradiated and nonirradiated rats (controls) were exposed to 25-min global ischemia followed by 60-min IR, or hearts were perfused without IR for the same protocol duration [time controls (TC)]. Online fluorometry of metabolic indices [redox state: reduced nicotinamide adenine dinucleotide (NADH), oxidized flavin adenine dinucleotide (FAD), and NADH/FAD redox ratio] and functional variables [systolic left ventricular pressure (LVP), diastolic LVP (diaLVP), coronary flow (CF), and heart rate were recorded in the beating heart; developed LVP (dLVP) and rate pressure product (RPP)] were derived. At the end of each experimental protocol, hearts were immediately snap frozen in liquid N2 for later three-dimensional imaging of the mitochondrial redox state using optical cryoimaging. Irradiation caused a delay in recovery of dLVP and RPP after IR when compared to nonirradiated hearts but recovered to the same level at the end of reperfusion. CF in the irradiated hearts recovered better than the control hearts after IR injury. Both fluorometry and 3-D cryoimaging showed that in WTI and control hearts, the redox ratio increased during ischemia (reduced) and decreased on reperfusion (oxidized) when compared to their respective TCs; however, there was no significant difference in the redox state between WTI and controls. In conclusion, our results show that although irradiation of rat hearts compromised baseline cardiovascular function, it did not alter cardiac mitochondrial redox state and induce greater susceptibility of these hearts to IR injury.
© 2018 Society of Photo-Optical Instrumentation Engineers (SPIE)
Mette Funding la Cour, Mette Funding la Cour, Shima Mehrvar, Shima Mehrvar, James S. Heisner, James S. Heisner, Mohammad Masoudi Motlagh, Mohammad Masoudi Motlagh, Meetha M. Medhora, Meetha M. Medhora, Mahsa Ranji, Mahsa Ranji, Amadou K. S. Camara, Amadou K. S. Camara, } "Optical metabolic imaging of irradiated rat heart exposed to ischemia–reperfusion injury," Journal of Biomedical Optics 23(1), 016011 (19 January 2018). https://doi.org/10.1117/1.JBO.23.1.016011 . Submission: Received: 31 August 2017; Accepted: 12 December 2017
Received: 31 August 2017; Accepted: 12 December 2017; Published: 19 January 2018
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