Affiliation:
1. Service d'Anesthésie Réanimation, Hôpital Cardiologique Louis Pradel;
2. Institut National de la Santé et de la Recherche Médicale E0226, Faculté de Médecine Lyon Nord, Université Claude Bernard Lyon I; and
3. Laboratoire de Biochimie, Hôpital Cardiologique Louis Pradel, 69394 Lyon Cedex 03, France
Abstract
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. Plasma catecholamine levels were measured at several time points. Although it dramatically increase plasma catecholamine levels, BD failed to reduce infarct size that averaged 0.49 ± 0.34 without BD versus 0.45 ± 0.27 g with BD. IPC and Iso, alone as well as after BD, significantly reduced infarct size that averaged 0.11 ± 0.04, 0.21 ± 0.15, 0.10 ± 0.09, and 0.22 ± 0.10 g in IPC, Iso, BD + IPC, and BD + Iso groups, respectively (means ± SD, P < 0.05 vs. controls). BD-induced catecholamines “storm” does not precondition the rabbit heart that however retains the ability to be protected by repetition of brief ischemia or isoflurane inhalation.
Publisher
American Physiological Society
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Cited by
15 articles.
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