Recipient hypertonic saline infusion prevents cardiac allograft dysfunction.

Objective: Hypertonic 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. Methods: Heart 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)-alpha expression was measured. Results: Weaning 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- a increased following transplantation, whereas HTS therapy attenuated IL production (P < .001). Transplantation increased plasma TNF-alpha levels and LV TNF-alpha expression, whereas HTS prevented this up-regulation (P <. 001). Conclusions: Recipient 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.