Ischemic preconditioning is not additive to preservation with hypothermia or crystalloid cardioplegia in the globally ischemic rat heart

Juggi, J. S.; Al-Awadi, Farida; Joseph, Shaji; Telahoun, G.; Prahash, Arun

doi:10.1007/978-1-4615-5765-4_39

Cited by 8 publications

(3 citation statements)

References 17 publications

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“…However, evaluation of pre-conditioning to protect hearts submitted to prolonged cold cardioplegic arrest has shown controversial results. 18,19 As expected, we showed that uncontrolled reperfusion after cold cardioplegia and 8 hours of global hypothermic ischemia induced significant reperfusion injury, Performing post-conditioning in the early period of reperfusion blunted this irreversible damage. This protection was efficient as early as 10 minutes after re-flow and was maintained throughout the reperfusion period (see Figure 1).…”

Section: Discussionsupporting

confidence: 52%

Post-conditioning Protects From Cardioplegia and Cold Ischemia via Inhibition of Mitochondrial Permeability Transition Pore

Ferrera

Bopassa

Angoulvant

et al. 2007

The Journal of Heart and Lung Transplantation

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Section: Discussionsupporting

confidence: 52%

Post-conditioning Protects From Cardioplegia and Cold Ischemia via Inhibition of Mitochondrial Permeability Transition Pore

Ferrera

Bopassa

Angoulvant

et al. 2007

The Journal of Heart and Lung Transplantation

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“…In one isolated rat heart study, IPC added to the protection of ischemia at 20°C (11); in another study, IPC did not improve postischemic function after 3.5 h of ischemia at 6°C (42). In other studies using isolated rat hearts, IPC improved cardiac function after 75 min of ischemia at 23°C, but not after 5 h of ischemia at 6°C (40), and improved function after 1 h of ischemia at 34°C, but not after 1 h of ischemia at 10°C (25). Our studies offer a partial answer for these different results.…”

Section: Discussionmentioning

confidence: 94%

Warm ischemic preconditioning improves mitochondrial redox balance during and after mild hypothermic ischemia in guinea pig isolated hearts

An¹,

Camara²,

Rhodes³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Ischemic preconditioning (IPC) induces distinctive changes in mitochondrial bioenergetics during warm (37 degrees C) ischemia and improves function and tissue viability on reperfusion. We examined whether IPC before 2 h of hypothermic (27 degrees C) ischemia affords additive cardioprotection and improves mitochondrial redox balance assessed by mitochondrial NADH and flavin adenine dinucleotide (FAD) autofluorescence in intact hearts. A mediating role of ATP-sensitive K(+) (K(ATP)) channel opening was investigated. NADH and FAD fluorescence was measured in the left ventricular wall of guinea pig isolated hearts assigned to five groups of eight animals each: hypothermia alone, hypothermia with ischemia, IPC with cold ischemia, 5-hydroxydecanoic acid (5-HD) alone, and 5-HD with IPC and cold ischemia. IPC consisted of two 5-min periods of warm global ischemia spaced 5 min apart and 15 min of reperfusion before 2 h of ischemia at 27 degrees C and 2 h of warm reperfusion. The K(ATP) channel inhibitor 5-HD was perfused from 5 min before until 5 min after IPC. IPC before 2 h of ischemia at 27 degrees C led to better recovery of function and less tissue damage on reperfusion than did 27 degrees C ischemia alone. These improvements were preceded by attenuated increases in NADH and decreases in FAD during cold ischemia and the reverse changes during warm reperfusion. 5-HD blocked each of these changes induced by IPC. This study indicates that IPC induces additive cardioprotection with mild hypothermic ischemia by improving mitochondrial bioenergetics during and after ischemia. Because effects of IPC on subsequent changes in NADH and FAD were inhibited by 5-HD, this suggests that mitochondrial K(ATP) channel opening plays a substantial role in improving mitochondrial bioenergetics throughout mild hypothermic ischemia and reperfusion.

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“…In studies on mild hypothermia, IPC (one cycle, 2 min of global ischemia plus 5 min of reperfusion at 37°C) improved cardiac function after 75 min of global ischemia at 23°C, but not after 5 h of cold ischemia at 6°C in isolated rat hearts (28). IPC (two cycles, 5 min of global ischemia and 10 min of reperfusion at 34°C) improved postischemic cardiac function in isolated rat hearts after 60 min of global ischemia at 34°C but not after 60 min of ischemia at 10°C (9). IPC in vivo rats also showed additive cardioprotection with mild hypothermia (8,34).…”

Section: Ipc and Hypothermic Ischemia-reperfusion Injurymentioning

confidence: 98%

Cardiac preconditioning with 4-h, 17°C ischemia reduces [Ca²⁺]_i load and damage in part via K_ATP channel opening

Chen

Camara²,

An³

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Brief ischemia before normothermic ischemia protects hearts against reperfusion injury (ischemic preconditioning, IPC), but it is unclear whether it protects against long-term moderate hypothermic ischemia. We explored in isolated guinea pig hearts 1) the influence of two 2-min periods of normothermic ischemia before 4 h, 17 degrees C hypothermic ischemia on cardiac cytosolic [Ca(2+)], mechanical and metabolic function, and infarct size, and 2) the potential role of K(ATP) channels in eliciting cardioprotection. We found that IPC before 4 h moderate hypothermia improved myocardial perfusion, contractility, and relaxation during normothermic reperfusion. Protection was associated with markedly reduced diastolic [Ca(2+)] loading throughout both hypothermic storage and reperfusion. Global infarct size was markedly reduced from 36 +/- 2 (SE)% to 15 +/- 1% with IPC. Bracketing ischemic pulses with 200 microM 5-hydroxydecanoic acid or 10 microM glibenclamide increased infarct size to 28 +/- 3% and 26 +/- 4%, respectively. These results suggest that brief ischemia before long-term hypothermic storage adds to the cardioprotective effects of hypothermia and that this is associated with decreased cytosolic [Ca(2+)] loading and enhanced ATP-sensitive K channel opening.

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Ischemic preconditioning is not additive to preservation with hypothermia or crystalloid cardioplegia in the globally ischemic rat heart

Cited by 8 publications

References 17 publications

Post-conditioning Protects From Cardioplegia and Cold Ischemia via Inhibition of Mitochondrial Permeability Transition Pore

Post-conditioning Protects From Cardioplegia and Cold Ischemia via Inhibition of Mitochondrial Permeability Transition Pore

Warm ischemic preconditioning improves mitochondrial redox balance during and after mild hypothermic ischemia in guinea pig isolated hearts

Cardiac preconditioning with 4-h, 17°C ischemia reduces [Ca²⁺]_i load and damage in part via K_ATP channel opening

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Ischemic preconditioning is not additive to preservation with hypothermia or crystalloid cardioplegia in the globally ischemic rat heart

Cited by 8 publications

References 17 publications

Post-conditioning Protects From Cardioplegia and Cold Ischemia via Inhibition of Mitochondrial Permeability Transition Pore

Post-conditioning Protects From Cardioplegia and Cold Ischemia via Inhibition of Mitochondrial Permeability Transition Pore

Warm ischemic preconditioning improves mitochondrial redox balance during and after mild hypothermic ischemia in guinea pig isolated hearts

Cardiac preconditioning with 4-h, 17°C ischemia reduces [Ca2+]i load and damage in part via KATP channel opening

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Cardiac preconditioning with 4-h, 17°C ischemia reduces [Ca²⁺]_i load and damage in part via K_ATP channel opening