TY - JOUR
T1 - Mitochondrial function during ischemic preconditioning
AU - Crestanello, Juan A.
AU - Doliba, Nicolai M.
AU - Babsky, Andriy M.
AU - Doliba, Natalia M.
AU - Niibori, Koki
AU - Osbakken, Mary D.
AU - Whitman, Glenn J.R.
N1 - Funding Information:
Partially supported by NIH Grant RO 1-HL39208 (MDO).
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2002
Y1 - 2002
N2 - Background. Ischemic preconditioning (IPC) protects the myocardium from ischemia reperfusion injury. The effect of IPC on the mitochondria is not well known. However, one of the mechanisms postulated in IPC (the opening of the mitochondrial KAATP channels) is likely to result in changes in mitochondrial function. Therefore, the purpose of this study was to determine the effect of IPC on mitochondrial function during ischemia reperfusion. Methods. Isolated rat hearts (n = 6/group) were subjected to (1) 30 minutes of equilibration, 25 minutes of ischemia, and 30 minutes of reperfusion (RP) (control group) or (2) 10 minutes of equilibration, two-5 minute episodes of IFC (each followed by 5 minutes of re-equilibration), 25 minutes of ischemia, and 30 minutes of RP (IPC group). Left ventricular rate pressure product (RPP) was measured. At end-equilibration (end-EQ) and at end-reperfusion (end-RP) mitochondria were isolated. Mitochondrial respiratory function (state 2, 3, and 4), respiratory control index (RCI), rate of oxidative phosphorylation (ADP/Δt), and ADP:O ratio were measured by polarography with the use of NADH- or FADH-dependent substrates. Results. IPC improved recovery of RPP at end-RP (72% ± 5% in IPC vs 30% ± 4% in control, P < .05). Ischemia reperfusion (IR) decreased state 3, ADP/Δt, and RCI in both groups compared with end-EQ. IPC improved state 3 (47 ± 3 in IPC vs 37 ± 2 ng-atoms O/min/mg protein in control), ADP/Δt (17 ± 1 in IPC vs 13 ± 1 nmol/s/mg protein in control), and RCI (3.7 ± 0.1 in IPC vs 2.1 ± 0.2 in control) at end-RP compared with control with the use of NADH-dependent substrate (P < .05 vs control). IPC also improved state 3 (85 ± 6 in IPC vs 71 ± 4 ng-atoms O/min/mg protein in control), ADP/Δt (18 ± 2 in IPC vs 12 ± 1 nmol/s/mg protein in control), RCI (2 ± 0.1 in IPC vs 1.5 ± 0.1 in control), and ADP:O ratios (1.4 ± 0.04 in IPC vs 1.7 ± 0.09 in control) at end-RP compared with control with the use of EADH-dependent substrate (P < .05 vs control). Conclusions. The cardioprotective effects of IPC can be attributed at least in part to the preservation of mitochondrial function during reperfusion.
AB - Background. Ischemic preconditioning (IPC) protects the myocardium from ischemia reperfusion injury. The effect of IPC on the mitochondria is not well known. However, one of the mechanisms postulated in IPC (the opening of the mitochondrial KAATP channels) is likely to result in changes in mitochondrial function. Therefore, the purpose of this study was to determine the effect of IPC on mitochondrial function during ischemia reperfusion. Methods. Isolated rat hearts (n = 6/group) were subjected to (1) 30 minutes of equilibration, 25 minutes of ischemia, and 30 minutes of reperfusion (RP) (control group) or (2) 10 minutes of equilibration, two-5 minute episodes of IFC (each followed by 5 minutes of re-equilibration), 25 minutes of ischemia, and 30 minutes of RP (IPC group). Left ventricular rate pressure product (RPP) was measured. At end-equilibration (end-EQ) and at end-reperfusion (end-RP) mitochondria were isolated. Mitochondrial respiratory function (state 2, 3, and 4), respiratory control index (RCI), rate of oxidative phosphorylation (ADP/Δt), and ADP:O ratio were measured by polarography with the use of NADH- or FADH-dependent substrates. Results. IPC improved recovery of RPP at end-RP (72% ± 5% in IPC vs 30% ± 4% in control, P < .05). Ischemia reperfusion (IR) decreased state 3, ADP/Δt, and RCI in both groups compared with end-EQ. IPC improved state 3 (47 ± 3 in IPC vs 37 ± 2 ng-atoms O/min/mg protein in control), ADP/Δt (17 ± 1 in IPC vs 13 ± 1 nmol/s/mg protein in control), and RCI (3.7 ± 0.1 in IPC vs 2.1 ± 0.2 in control) at end-RP compared with control with the use of NADH-dependent substrate (P < .05 vs control). IPC also improved state 3 (85 ± 6 in IPC vs 71 ± 4 ng-atoms O/min/mg protein in control), ADP/Δt (18 ± 2 in IPC vs 12 ± 1 nmol/s/mg protein in control), RCI (2 ± 0.1 in IPC vs 1.5 ± 0.1 in control), and ADP:O ratios (1.4 ± 0.04 in IPC vs 1.7 ± 0.09 in control) at end-RP compared with control with the use of EADH-dependent substrate (P < .05 vs control). Conclusions. The cardioprotective effects of IPC can be attributed at least in part to the preservation of mitochondrial function during reperfusion.
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U2 - 10.1067/msy.2002.119490
DO - 10.1067/msy.2002.119490
M3 - Article
C2 - 11854695
AN - SCOPUS:0036183675
VL - 131
SP - 172
EP - 178
JO - Surgery
JF - Surgery
SN - 0039-6060
IS - 2
ER -