Beta-adrenergic Receptor Antagonism Preserves Myocardial Function After Brain Death in a Porcine Model

McLean, Karen; Pandalai, Prakash K.; Pearl, Jeffrey M.; Bulcao, Christian F.; Lyons, Jefferson M.; Wagner, Connie J.; Akhter, Shahab A.; Duffy, Jodie Y.

doi:10.1016/j.healun.2007.01.034

Cited by 12 publications

(6 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our method of attenuating brain death–induced ventricular dysfunction did not result in the same degree of preservation as previous studies that were able to completely prevent deterioration in ventricular function; 21,25 however, the former study 21 required administration of a beta-blocker before the induction of brain death and the latter study 25 required administration of steroids either before or only 1 hour after induction of brain death, requirements that may diminish their clinical relevance.…”

Section: Discussionmentioning

confidence: 78%

“…Our data from the brain death group are consistent with previous work examining the effect of brain death on the same indices of myocardial performance in pigs both in terms of the extent of dysfunction and the time course of its development. 21 To our knowledge, this is the first time the CytoSorb HA device has been used in the context of brain death in an experimentally controlled setting where its impact on organ function has been evaluated. The efficacy of cytokine HA appeared more effective for TNF than for IL-6, where the trend in diminished IL-6 expression in the brain dead treatment group did not reach statistical significance; however, the physiologic response to brain death is notoriously unpredictable, resulting in large standard errors of the mean, thus making demonstrations of differences between groups challenging in a small preliminary study such as this one.…”

Section: Discussionmentioning

confidence: 94%

See 1 more Smart Citation

Effect of cytokine hemoadsorption on brain death–induced ventricular dysfunction in a porcine model

Mikhova

Don

Laflamme

et al. 2013

The Journal of Thoracic and Cardiovascular Surgery

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 94%

Effect of cytokine hemoadsorption on brain death–induced ventricular dysfunction in a porcine model

Mikhova

Don

Laflamme

et al. 2013

The Journal of Thoracic and Cardiovascular Surgery

View full text Add to dashboard Cite

show abstract

“…Thus, McLean et al (10) found that IL‐6, IL‐10, and the intercellular adhesion molecule, ICAM‐1 were higher in the left ventricle in brain‐dead pigs than in sham operated ones. However, the mean blood pressure was reported to be 32 mmHg at 1 and 6 h after induction of brain death in two studies from the same group (19, 20).…”

Section: Discussionmentioning

confidence: 99%

Does brain death induce a pro‐inflammatory response at the organ level in a porcine model?

Barklin¹,

Larsson²,

Vestergaard³

et al. 2008

Acta Anaesthesiol Scand

View full text Add to dashboard Cite

show abstract

“…L'orage végétatif observé lors du passage en ME est susceptible d'induire une cardiopathie de stress (ou cardiopathie adrénergique), notamment secondaire à une surstimulation des récepteurs β -adrénergiques [39][40][41]. Le caractère potentiellement réver-sible de cette dysfonction est en faveur d'une sidération myocardique s'intégrant dans une cardiopathie de stress.…”

Section: Dysfonction Myocardiqueunclassified

“…Dans des études animales expérimentales, un traitement préventif basé sur l'administration de β-bloquants avant la survenue de « l'orage catécholaminergique » pourrait permettre de limiter la désensibilisation des récepteurs bé ta-adrénergiques et d'éviter de fait la survenue d'une dysfonction contractile [39][40][41]. Cette stratégie reste à évaluer par une étude clinique.…”

Section: Traitement De L'orage Catécholaminergiqueunclassified

Conséquences cardiovasculaires de la mort cérébrale et prise en charge pour prélèvement d’organe(s)

Champigneulle

Charpentier

2015

Réanimation

View full text Add to dashboard Cite

La mort encéphalique (ME) est susceptible d'entraîner une dysfonction cardiocirculatoire, par l'intermé-diaire de différents mécanismes résultant de l'ischémie céré-brale : orage catécholaminergique, dysfonction neurohormonale et inflammation systémique. Cette dysfonction cardiovasculaire est potentiellement exacerbée par les anté-cédents du potentiel donneur décédé en mort encéphalique (DDME) et le contexte clinique dans lequel survient la ME. La détection et la prise en charge d'une défaillance hémo-dynamique survenant dans ce contexte sont cruciales dans le but de préserver la viabilité des greffons potentiels, mais aussi de tenter d'en améliorer la qualité et d'en augmenter le nombre. Cette prise en charge hémodynamique nécessite de connaître la physiopathologie de la ME et d'utiliser un monitorage. Elle repose sur l'administration d'agents inotropes en cas de dysfonction myocardique, la correction d'une hypovolémie et l'administration d'amines vasopressives. En l'état actuel, une opothérapie substitutive (hormones thyroï-diennes, glucocorticoïdes) ne peut être recommandée. Les principales mesures associées indispensables sont : la correction des désordres électrolytiques et métaboliques, la lutte contre l'hypothermie et le traitement d'un diabète insipide. Une réanimation « agressive » du potentiel DDME doit être poursuivie jusqu'au clampage aortique au bloc opératoire. Le sujet en ME, potentiel donneur d'organe(s), doit être considéré comme un « patient » de réanimation à part entière. Mots clés Mort encéphalique · Prélèvement d'organe · Réanimation · Gestion hémodynamiqueAbstract During brain death (BD) process, several mechanisms may induce cardio-circulatory failure. These mechanisms are secondary to brain ischemia and involve a catecholamine storm, a systemic inflammatory state and a hormonal dysfunction. Donor past history and associated medical context may worsen the hemodynamic failure. Objectives of early recognition and treatment of cardiocirculatory failure in potentials BD donors are: to preserve the viability of the potential grafts, to improve organ's function and to increase the number of recovered organs. Hemodynamic resuscitation is principally based on the use of inotropic agents in case of myocardial dysfunction, the correction of hypovolemia and the use of vasopressors (norepinephrine) adapted using a cardiovascular monitorage. Systematic hormone therapy is still debated. Associated supportive treatment includes correction of metabolic and electrolytic disorders, avoidance of hypothermia and management of diabetes insipidus. Aggressive management must be conducted until aortic clamping during organ recovery in operating room. Potential BD donor must be managed like any other intensive care unit patient.

show abstract

Beta-adrenergic Receptor Antagonism Preserves Myocardial Function After Brain Death in a Porcine Model

Cited by 12 publications

References 36 publications

Effect of cytokine hemoadsorption on brain death–induced ventricular dysfunction in a porcine model

Effect of cytokine hemoadsorption on brain death–induced ventricular dysfunction in a porcine model

Does brain death induce a pro‐inflammatory response at the organ level in a porcine model?

Conséquences cardiovasculaires de la mort cérébrale et prise en charge pour prélèvement d’organe(s)

Contact Info

Product

Resources

About