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Published on: May 21, 2019
Effect of cytokine hemoadsorption on brain death-induced ventricular dysfunction in a porcine model
Krasimira M Mikhova1, Creighton W Don, Michael Laflamme
1Division of Cardiothoracic Surgery, University of Washington Medical Center, Seattle, Wash, USA.
Insights
Hemoadsorption of cytokines can reduce brain death-induced heart dysfunction in pigs. This extracorporeal therapy shows promise for improving cardiac donor viability and expanding the donor pool.
Area of Science:
- Cardiology
- Transplantation Immunology
- Critical Care Medicine
Background:
- Brain death can lead to rapid cardiac dysfunction, limiting the availability of donor hearts for transplantation.
- Elevated cytokine levels contribute to myocardial damage and impaired ventricular function following brain death.
- Expanding the cardiac donor pool is crucial for meeting the growing demand for heart transplantation.
Purpose of the Study:
- To investigate whether hemoadsorption of cytokines can attenuate ventricular dysfunction induced by brain death.
- To evaluate the impact of cytokine hemoadsorption on cardiac function and myocardial water content in a porcine model.
Main Methods:
- Eighteen Yorkshire pigs underwent instrumentation for left ventricular function assessment.
- Brain death was induced via intracranial balloon inflation, with a control group and a hemoadsorption group.
- Cytokine levels, preload recruitable stroke work, and diastolic relaxation constant (tau) were measured hourly for 6 hours.
Main Results:
- Brain death significantly reduced preload recruitable stroke work and elevated tau, indicating ventricular dysfunction.
- Hemoadsorption of cytokines preserved cardiac function, with preload recruitable stroke work remaining at 80% of baseline.
- Myocardial water content was significantly higher in the brain death group compared to controls and the hemoadsorption group.
Conclusions:
- Extracorporeal cytokine hemoadsorption effectively attenuates brain death-induced ventricular dysfunction in a porcine model.
- This therapeutic approach may help improve the quality of cardiac allografts and expand the donor pool for transplantation.
- Further research is needed to fully elucidate the relationship between cytokine levels and functional improvements.
Objective:
In an effort to expand the cardiac donor pool, we tested the hypothesis that hemoadsorption of cytokines attenuates brain death-induced ventricular dysfunction.
Methods:
Eighteen Yorkshire pigs (50-60 kg) were instrumented with a left ventricular conductance catheter. Cytokine expression, preload recruitable stroke work, and the diastolic relaxation constant tau were measured at baseline and at hourly intervals for 6 hours after induction of brain death by intracranial balloon inflation (brain death, n = 6) or sham operation (control, n = 6). In a third group (brain death + hemoadsorption, n = 6), 3 hours after induction of brain death, animals were placed on an extracorporeal circuit containing a cytokine-hemoadsorption device for the remaining 3 hours of the experiment. Myocardial water content was measured after the animals were killed.
Results:
Six hours after induction of brain death, tumor necrosis factor and interleukin-6 were highest in the brain death group (106 ± 13.1 pg/mL and 301 ± 181 pg/mL, respectively), lowest in controls (68.3 ± 8.55 pg/mL and 37.8 ± 11 pg/mL, respectively), and intermediate in the brain death + hemoadsorption group (81.2 ± 35.2 pg/mL and 94.6 ± 20 pg/mL, respectively). Compared with controls, preload recruitable stroke work was significantly reduced in the brain death group 4 hours after the induction of brain death and was 50% of baseline by 5 hours. In the brain death + hemoadsorption group, preload recruitable stroke work was relatively preserved at 80% of baseline at similar time points. Tau remained unchanged in the control and brain death + hemoadsorption groups, whereas in the brain death group it was significantly elevated versus baseline 5 (139.3% ± 21.5%) and 6 (172% ± 16.1%) hours after induction of brain death. Myocardial water content was significantly greater in the brain death group than in the other 2 groups.
Conclusions:
Hemoadsorption of cytokines using an extracorporeal circuit attenuates brain death-induced ventricular dysfunction in a porcine model. Improvement in function generally correlates with trends in cytokine expression, but this relationship requires further investigation.
