Brain Death Does Not Change Epicardial Action Potentials and Their Response to Ischemia–Reperfusion in Open-chest Pigs

Christé, Georges; Hadour, Guylaine; Ovize, Michel; Ferrera, René

doi:10.1016/j.healun.2006.03.018

Cited by 3 publications

(4 citation statements)

References 30 publications

(31 reference statements)

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“…31 A second peak was observed 45 minutes after BD in one study 32 and even several hours after death in another study. 25,33 This later catecholamine surge could be attributed to the adrenal response to BD, as suggested by investigators such as Chen et al 31 In our series of BD donors, catecholamine levels above normal were detected in most cases. Our results clearly reflect the expected release profile for epinephrine, yet levels detected at the time of BD peaked at only 2.36-fold.…”

Section: Discussionsupporting

confidence: 64%

Brain Death Effects on Catecholamine Levels and Subsequent Cardiac Damage Assessed in Organ Donors

López

Otero

Moreno

et al. 2009

The Journal of Heart and Lung Transplantation

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Section: Discussionsupporting

confidence: 64%

Brain Death Effects on Catecholamine Levels and Subsequent Cardiac Damage Assessed in Organ Donors

López

Otero

Moreno

et al. 2009

The Journal of Heart and Lung Transplantation

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“…Even though the time elapsed for delivery of 3 pulses with 30 ms duration would be shorter that the reported action potential duration recorded in vitro in swine ventricle at physiological temperatures (> 100 ms; Roscher et al, 2001), it is possible that the in vivo conditions, such as transient myocardial ischemia and increased catecholamine release, resulting from the interruption of cardiac pumping during VF, may have resulted in action potential shortening (Christé et al, 2006;Hoeker et al, 2014). In this case, it is likely that defibrillatory pulses would reach some cells during the relative refractory period (vulnerable period), which would favor arrhythmia reinitiation (Corbisiero et al, 1999), thus masking or even reverting the beneficial effect of multidirectional defibrillation.…”

Section: Discussionmentioning

confidence: 88%

System for open-chest, multidirectional electrical defibrillation

et al. 2016

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Introduction: Cardiomyocytes are more sensitive to stimulatory electrical fields when the latter are applied longitudinally to the cell major axis. In the whole heart, cells have different spatial orientations, which may limit the effectiveness of conventional electrical defibrillation (i.e., shock delivery in a single direction). This article describes the constructive aspects of a portable system for rapidly-switching, multidirectional stimulus delivery, composed of an electrical defibrillator and multielectrode-bearing paddles for direct cardiac defibrillation. Methods:The defibrillator delivers monophasic, truncated monoexponential waveforms with energy up to 7.3 J. Upon selection of the defibrillation modality (unidirectional or multidirectional), shock delivery is triggered through 1 or 3 outputs. In the latter case, triggering is sequentially switched to the outputs, without interval or temporal overlap. Each paddle contains 3 electrodes that define shock pathways spaced by 60°. The system was tested in vivo for reversal of experimentally-induced ventricular fibrillation in healthy swine, using 30-and 20-ms long shocks (N= 4 in each group). Results: The defibrillator delivers identical stimulus waveforms through all outputs in both stimulation modalities. In all animals, successful defibrillation required lower shock energy when 20 ms-long stimuli were applied in 3 directions, compared to a single direction. However, performance was poorer with multidirectional defibrillation for 30 ms-long shocks. Conclusion: The delivery of identical shock waveforms allowed confirmation that multidirectional defibrillation can promote restoration of sinus rhythm with lower shock energy, which may reduce myocardial electrical damage during defibrillation. Nevertheless, increase in shock duration greatly impairs the effectiveness of this defibrillation modality.

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“…To our knowledge, comparative data of cellular electrophysiological properties of brain‐dead versus fresh pig hearts have not been reported. In a previous study using surface electrodes on cardiac muscle during a 3 h brain‐dead period, 8 it was found that the action potential or ischemia responses were not affected. Our studies include a longer brain‐dead period and a period in cardioplegia closer to the clinical situation, and it is possible that we identify changes in the myocardium that are not detectable on the epicardial surface or that develop at later stages, that is, after more than 3 h.…”

Section: Discussionmentioning

confidence: 94%

“…Also, studies of excitation‐contraction in the myocardium are few. Experiments on 3‐h brain death in pigs have suggested that no major changes in epicardial action potential occur 8 . Further characterization of coronary vessels and myocardium of the brain‐dead heart is needed.…”

Section: Introductionmentioning

confidence: 99%

Excitation and contraction of cardiac muscle and coronary arteries of brain‐dead pigs

Arlock

Davis

et al. 2022

FASEB BioAdvances

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Excitability and contraction of cardiac muscle from brain‐dead donors critically influence the success of heart transplantation. Membrane physiology, Ca2+‐handling, and force production of cardiac muscle and the contractile properties of coronary arteries were studied in hearts of brain‐dead pigs. Cardiac muscle and vascular function after 12 h brain death (decapitation between C2 and C3) were compared with properties of fresh tissue. In both isolated cardiomyocytes (whole‐cell patch clamp) and trabecular muscle (conventional microelectrodes), action potential duration was shorter in brain dead, compared to controls. Cellular shortening and Ca2+ transients were attenuated in the brain dead, and linked to lower mRNA expression of L‐type calcium channels and a slightly lower ICa,L, current, as well as to a lower expression of phospholamban. The current–voltage relationship and the current above the equilibrium potential of the inward K+ (IK1) channel were altered in the brain‐dead group, associated with lower mRNA expression of the Kir2.2 channel. Delayed K+ currents were detected (IKr, IKs) and were not different between groups. The transient outward K+ current (Ito) was not observed in the pig heart. Coronary arteries exhibited increased contractility and sensitivity to the thromboxane analogue (U46619), and unaltered endothelial relaxation. In conclusion, brain death involves changes in cardiac cellular excitation which might lower contractility after transplantation. Changes in the inward rectifier K+ channel can be associated with an increased risk for arrhythmia. Increased reactivity of coronary arteries may lead to increased risk of vascular spasm, although endothelial relaxant function was well preserved.

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Brain Death Does Not Change Epicardial Action Potentials and Their Response to Ischemia–Reperfusion in Open-chest Pigs

Cited by 3 publications

References 30 publications

Brain Death Effects on Catecholamine Levels and Subsequent Cardiac Damage Assessed in Organ Donors

Brain Death Effects on Catecholamine Levels and Subsequent Cardiac Damage Assessed in Organ Donors

System for open-chest, multidirectional electrical defibrillation

Excitation and contraction of cardiac muscle and coronary arteries of brain‐dead pigs

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