Author + information
- Jonas Agerlund Povlsen,
- Bo Løfgren,
- Christian Dalgas,
- Nichlas R. Jespersen,
- Jacob Johnsen and
- Hans Erik Bøtker
The aim of the present study was to characterize the dynamics of reperfusion injury by portraying the temporal release of lactate dehydrogenase (LDH) during ischemia-reperfusion (IR) injury in an isolated heart model.
We studied infarct size (IS) and LDH release in three groups: I) Effect of reperfusion length was evaluated in 79 rats subjected to 40 min ischemia and 60, 90, 120 or 180 min reperfusion and ischemic preconditioning (IPC) or no IPC (Con). II) Differentiation between ischemia and reperfusion injury was studied in 21 rats subjected to prolonged ischemia (PI) (60 min) or ischemic postconditioning (PC) (6 × 10+10s) at onset of reperfusion. III) Modification of IR-injury was studied by activation of Reperfusion Injury Salvage Kinase Pathway (RISK) and inhibition of mitochondrial Permeability Transition Pore (mPTP) in 42 rats subjected to IPC+Wortmannin (RISK-inhibitor), Con+lnsulin (RISK-activator) or Con+Cyclosporin A (mPTP inhibitor).
IS increased from 60 to 120 min reperfusion in Con hearts. LDH was released in two separate peaks during reperfusion from 3–20 (P1) and 45–120 min (P2) of reperfusion (Figure). IPC attenuated both peaks. PC decreased P2. PI increased P1. RISK activation attenuated both P1 and P2, while mPTP inhibition only decreased P2.
LDH release during IR is separated in two distinct peaks that reflect ischemic and reperfusion injury. Modification of each peak separately reflects targeted intervention against ischemia and reperfusion.
Poster Sessions, Expo North
Monday, March 11, 2013, 9:45 a.m.-10:30 a.m.
Session Title: Acute Coronary Syndromes: Basic V
Abstract Category: 2. Acute Coronary Syndromes: Basic
Presentation Number: 1300-192
- 2013 American College of Cardiology Foundation