• J. Thorac. Cardiovasc. Surg. · Feb 2019

    Recipient hypertonic saline infusion prevents cardiac allograft dysfunction.

    • Roberto V P Ribeiro, Mitesh V Badiwala, Danny Ramzy, Laura C Tumiati, and Vivek Rao.
    • Heart Transplant Program, Peter Munk Cardiac Centre, Toronto General Hospital, University Health Network, Division of Cardiovascular Surgery, University of Toronto, Toronto, Ontario, Canada.
    • J. Thorac. Cardiovasc. Surg. 2019 Feb 1; 157 (2): 615-625.e1.

    ObjectiveHypertonic saline (HTS) has potent immune and vascular effects. We assessed recipient pretreatment with HTS on allograft function in a porcine model of heart transplantation and hypothesized that HTS infusion would limit endothelial and left ventricular (LV) dysfunction following transplantation.MethodsHeart transplants were performed after 6 hours of cold ischemic storage. Recipient pigs were randomized to treatment with or without HTS (7.5% NaCl) before cardiopulmonary bypass (CPB). Using a myograft apparatus, coronary artery endothelial-dependent (Edep) and -independent (Eind) relaxation was assessed. LV performance was determined using pressure-volume loop analysis. Pulmonary interleukin (IL)-2, IL-6, and tumor necrosis factor (TNF)-α expression was measured.ResultsWeaning from CPB and LV performance after transplantation were improved in HTS-treated animals. Successful weaning from CPB was greater in the HTS-treated hearts (8 of 8 vs 2 of 8; P < .05). Mean LV functional recovery was improved in the HTS-treated animals, as assessed by preload recruitable stroke work (65 ± 10% vs 27 ± 10%; P < .001) and end-systolic elastance (55 ± 7% vs 37 ± 4%; P < .001). Treatment with HTS resulted in improved Edep (mean maximum elastance [Emax], 56 ± 5% vs 37 ± 7%; P < .001) and Eind (mean Emax%, 77 ± 6% vs 52 ± 4%; P < .001) vasorelaxation compared with control. Pulmonary expression of IL-2, IL-6, and TNF-α increased following transplantation, whereas HTS therapy attenuated IL production (P < .001). Transplantation increased plasma TNF-α levels and LV TNF-α expression, whereas HTS prevented this up-regulation (P < .001).ConclusionsRecipient HTS pretreatment preserves allograft vasomotor and LV function, and HTS therapy limits CPB-induced injury. HTS may be a novel recipient intervention to prevent graft dysfunction.Copyright © 2018 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.

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