Brain death provokes very acute alteration in myocardial morphology detected by echocardiography: preventive effect of beta-blockers.

Our objective was to evaluate immediate acute changes in myocardial function during the autonomic storm of brain death (BD). Wistar rats were divided into four groups (n = 8/group): controls without any treatment, β-blocker (Esmolol®, 10 mg/kg), calcium channel blocker (Diltiazem®, 10 mg/kg), or alpha-blocker (Prazosin®, 0.3 mg/kg).

Brain death does not change epicardial action potentials and their response to ischemia-reperfusion in open-chest pigs.

Background: It is debated whether brain death (BD) causes transient functional ischemia. In this investigation we used monophasic action potential (AP) recording during BD as a sensitive means to assess: (i) whether ischemia was present; and (ii) the effect of BD on a subsequent ischemia-reperfusion challenge.

Methods: In Period 1, BD was induced (BD group, 6 pigs) or not induced (sham maneuver, control [C] group, 6 pigs), and effects were followed for 3 hours.

Stable myocardial function and endocrine dysfunction during experimental brain death.

Background: The origin of cardiac impairment during brain death (BD) is controversial. Using a pig experimental model we sought to assess hormonal changes during the first stage of brain death and how these changes contribute to hemodynamic alteration and myocardial dysfunction.

Methods: Twenty-two pigs were randomized into 2 groups: a control (C) group and a BD group.

Preservation of ischemia and isoflurane-induced preconditioning after brain death in rabbit hearts.

We sought to determine whether brain death-induced catecholamine release preconditions the heart, and if not, whether it precludes further protection by repetitive ischemia or isoflurane. Anesthetized rabbits underwent 30 min of coronary occlusion and 4 h of reperfusion. The effect on infarct size of either no intervention (controls), ischemic preconditioning (IPC), or isoflurane inhalation (Iso) was evaluated with or without previous brain death (BD) induced by subdural balloon inflation.

An optimal experimental design for the development of preservative heart solutions.

Background: The aim of this study was to determine the optimal composition of a new medium for long-term hypothermic heart preservation.

Methods: The independent effects of 19 compounds were evaluated using an in vitro porcine model. Tissue viability was assessed by measuring the reduction of methyltetrazolium salt, oxygen consumption and energetic compound levels on myocardial biopsies after 24-, 48- or 72-hour incubation periods.