Vol. 283, Issue 5, H1769-H1774, November 2002
Preservation of ischemia and isoflurane-induced
preconditioning after brain death in rabbit hearts
Pascal
Chiari1,
Vincent
Piriou1,
Guylaine
Hadour2,
Claire
Rodriguez3,
Joseph
Loufouat2,
Jean-Jacques
Lehot1,
Michel
Ovize2, and
René
Ferrera2
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
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.
catecholamines; volatile anesthetics; myocardium
