American Journal of Physiology-Heart and Circulatory Physiology · 2002 · 17 citations · 24 references
MedicineCardiologyPharmacologyAnesthesiaGeneral AnesthesiaNeuropharmacologyIschemic Heart DiseaseNeuroprotectionBalloon Inflation PressureBrain Death EvaluationInfarct ExpansionInfarct Size AssessmentInfarct Size QuantificationPreconditioning
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.
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Adrenergic effects on the biology of the adult mammalian cardiocyte.
Douglas L. Mann, Robert L. Kent, B Parsons et al. · Circulation · 1992 · 872 citations
Isoflurane Mimics Ischemic Preconditioning via Activation of KATPChannels
Judy R. Kersten, Todd J. Schmeling, Paul S. Pagel et al. · Anesthesiology · 1997 · 423 citations · Full text
Medicine, Cardiology, Pharmacology +12