Myocardial protection with postconditioning is not enhanced by ischemic preconditioning

Halkos, Michael E.; Kerendi, Faraz; Corvera, Joel S.; Wang, Ning-Ping; Kin, Hajime; Payne, Christopher; Sun, He-Ying; Guyton, Robert A.; Vinten‐Johansen, Jakob; Zhao, Zhi‐Qing

doi:10.1016/j.athoracsur.2004.03.033

Cited by 157 publications

(144 citation statements)

References 25 publications

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“…In postCI interruption of reperfusion after 1 hour of coronary artery occlusion in canine model (3 cycles of 30 s reperfusion followed by 30 s ischemia) followed by reperfusion for 3h reduced the size of cardiac infracted tissue 46,47 . Reducing size of infarcted area afforded by postCI has been observe in different species, including pigs, dogs, rabbits, mice and rats 41 .…”

Section: ■ Discussionmentioning

confidence: 99%

Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion

et al. 2018

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Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion 1 AbstractPurpose: To investigate the cardioprotective effects of ischemic preconditioning (preIC) and postconditioning (postIC) in animal model of cardiac ischemia/reperfusion. Methods: Adult rats were submitted to protocol of cardiac ischemia/reperfusion (I/R) and randomized into three experimental groups: cardiac I/R (n=33), preCI + cardiac I/R (n=7) and postCI + cardiac I/R (n=8). After this I/R protocol, the incidence of ventricular arrhythmia (VA), atrioventricular block (AVB) and lethality (LET) was evaluated using the electrocardiogram (ECG) analysis. Results: After reestablishment of coronary blood flow, we observed variations of the ECG trace with increased incidence of ventricular arrhythmia (VA) (85%), atrioventricular block (AVB) (79%), and increase of lethality (70%) in cardiac I/R group. The comparison between I/R + preIC group with I/R group demonstrated significant reduction in VA incidence to 28%, AVB to 0% and lethality to 14%. The comparison of I/R + postIC group with I/R group was observed significance reduction in AVB incidence to 25% and lethality to 25%. Conclusion:The preconditioning strategies produce cardioprotection more efficient that postconditioning against myocardial dysfunctions and lethality by cardiac ischemia and reperfusion.

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Section: ■ Discussionmentioning

confidence: 99%

Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion

et al. 2018

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“…Data from literature have suggested that ischemic postconditioning is powerful endogenous mechanism of cardioprotection, because it reduces the infracted area [5], endothelial dysfunction [5], adhesion of neutrophils to vascular endothelium [6], formation of reactive oxygen species [27], reperfusion arrhythmias [15.27], myocardial edema [7] and apoptosis [6] and may require major change in the paradigms of myocardial protection.…”

Section: Discussionmentioning

confidence: 99%

Efeitos do pós-condicionamento isquêmico na função ventricular esquerda de corações isolados de ratos

Pinheiro¹,

Fiorelli²,

Gomes³

2009

Rev Bras Cir Cardiovasc

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Efeitos do pós-condicionamento isquêmico na função ventricular esquerda de corações isolados de ratosEffects of ischemic postconditioning on left ventricular function of isolated rat hearts Abstract Objective: To assess the effects of ischemic postconditioning on left ventricular function in isolated rat hearts.Methods: Twenty-four Wistar rats were used. These hearts underwent perfusion by modified LANGERDORFF method and distributed into three groups: GI -control (n=8); GII -three cycles of postconditioning of 10/10s (n=8); GIIIthree cycles of postconditioning of 30/30s (n=8). After a 15min stabilization period, all hearts underwent 20min of global ischemia following 20min of reperfusion. In the times 0 (control), 5, 10, 15 and 20min of reperfusion, the heart rate (HR), the coronary flow (CoF), the systolic pressure, the (+dP/dt max) contractility and (-dP/dt max) velocity of relaxation were measured. Data were analyzed by ANOVA method followed by Tukey's test for differences between groups and P < 0.05 was considered significant. Rev Bras Cir Cardiovasc 2009; 24(1): 31-37

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“…Nevertheless, the optimal duration of the reocclusion and reperfusion periods of POC is currently unknown, but this most likely differs between animal species. Thus, although POC with three 30-s periods of abrupt CAO, starting 30 s after the initial reperfusion and interspersed by 30 s of abrupt reperfusion, limited infarct size produced by a 60-min CAO in the dog (13,39), it failed to afford cardioprotection against a 30-min CAO in the rat (34). On the basis of this single observation, the authors suggested that briefer periods (i.e., 10 -15 s) of reocclusion and reperfusion are required in smaller than in larger animals, in which 30 s cycles are effective (34), but conclusive evidence for this hypothesis is lacking.…”

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confidence: 99%

Cardiac effects of postconditioning depend critically on the duration of index ischemia

Manintveld

Hekkert²,

Bos³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

100

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Postconditioning (POC) is known as the phenomenon whereby brief intermittent ischemia applied at the onset of reperfusion following index ischemia limits myocardial infarct size. Whereas there is evidence that the algorithm of the POC stimulus is an important determinant of the protective efficacy, the importance of the duration of index ischemia on the outcome of the effects of POC has received little attention. Pentobarbital sodiumanesthetized Wistar rats were therefore subjected to index ischemia produced by coronary artery occlusions (CAO) of varying duration (15-120 min) followed by reperfusion, without or with postconditioning produced by three cycles of 30-s reperfusion and reocclusion (3POC30). 3POC30 limited infarct size produced by 45-min CAO (CAO45) from 45 Ϯ 3% to 31 Ϯ 5%, and CAO60 from 60 Ϯ 3% to 47 Ϯ 6% (both P Յ 0.05). In contrast, 3POC30 increased infarct size produced by CAO15 from 3 Ϯ 1% to 19 Ϯ 6% and CAO30 from 36 Ϯ 6 to 48 Ϯ 4% (both P Յ 0.05). This deleterious effect of 3POC30 was not stimulus sensitive because postconditioning with 3POC5 and 3POC15 after CAO30 also increased infarct size. The cardioprotection by 3POC30 after CAO60 was accompanied by an increased stimulation of Akt phosphorylation at 7 min of reperfusion and a 36% lower superoxide production, measured by dihydroethidium fluorescence, after 2 h of reperfusion. Consistent with these results, cardioprotection by 3POC30 was abolished by phosphatidylinositol-3-OH-kinase inhibition, as well as nitric oxide (NO) synthase inhibition. The deleterious effect of 3POC30 after CAO15 was accompanied by an increased superoxide production with no change in Akt phosphorylation and was not affected by NO synthase inhibition. In conclusion, the effect of cardiac POC depends critically on the duration of the index ischemia and can be either beneficial or detrimental. These paradoxical effects of POC may be related to the divergent effects on Akt phosphorylation and superoxide production.

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Myocardial protection with postconditioning is not enhanced by ischemic preconditioning

Cited by 157 publications

References 25 publications

Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion

Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion

Efeitos do pós-condicionamento isquêmico na função ventricular esquerda de corações isolados de ratos

Cardiac effects of postconditioning depend critically on the duration of index ischemia

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