Characterisation of the infarct-limiting effect of delayed preconditioning: timecourse and dose-dependency studies in rabbit myocardium

Baxter, Gary F.; Goma, Fastone; Yellon, Derek M.

doi:10.1007/bf00788633

Cited by 179 publications

(82 citation statements)

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“…172,219 -221 Recent work suggests that the delayed anti-infarct effect of preconditioning may extend over a period of 1 to 3 days, unlike the early period of protection by classic preconditioning, which is lost within a few hours. 222 The mechanism of the delayed effect of preconditioning is under investigation. The time delay may allow activation of genes and expression of new proteins that could play a role in the late protection.…”

Section: Second Windowmentioning

confidence: 99%

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

et al. 1998

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Section: Second Windowmentioning

confidence: 99%

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

et al. 1998

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“…1 This phenomenon is known as the delayed phase or second window of preconditioning (SWOP). The delayed phase of preconditioning is preceded by an early phase, which is known to last 2 to 3 hours after the initial preconditioning insult.…”

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confidence: 99%

Inducible Nitric Oxide Synthase Mediates Delayed Myocardial Protection Induced by Activation of Adenosine A ₁ Receptors

et al. 2000

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Background-The mechanism of delayed preconditioning induced by activation of adenosine A 1 receptors (A 1 ARs) is not fully understood. We determined the role of inducible nitric oxide synthase (iNOS) in mediating adenosine-induced late cardioprotection using pharmacological inhibitors and iNOS gene-knockout mice. Methods and Results-Adult male mice were treated with saline or an A 1 AR agonist, 2-chloro-N 6 -cyclopentyladenosine (CCPA). Twenty-four hours later, the hearts were perfused in Langendorff mode and subjected to 30 minutes of global ischemia followed by 30 minutes of reperfusion. 8-Cyclopentyl-1,3-dipropylxanthine (DPCPX; 0.1 mg/kg IP) and S-methylisothiourea (SMT; 3 mg/kg IP) were used to block A 1 ARs and iNOS, respectively. Infarct size (IS) was measured by triphenyltetrazolium chloride staining, and iNOS expression was measured by Western blots. Myocardial IS was reduced from 24.0Ϯ3.2% in the saline group to 12.2Ϯ2.5% in CCPA-treated mice (PϽ0.05). The infarct-reducing effect of CCPA was abrogated by DPCPX (29.3Ϯ3.4%) and SMT (32.3Ϯ2.6%) and was absent in mice with targeted ablation of iNOS (23.9Ϯ1.6%). CCPA produced improvement in postischemic end-diastolic pressure, developed pressure, and rate-pressure product, which was also blocked by DPCPX and SMT. Increased iNOS protein expression observed in CCPA-treated hearts was diminished by DPCPX. Conclusions-Selective

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“…In contrast, delayed protection appears 12 to 24 hours after the initial stimulus and lasts 3 to 4 days in an intact heart, although the magnitude of protection may be less than that in the early phase (1,21,43). Signaling molecules trigger development of delayed protection by activating a series of complex downstream events that ultimately result in activation of cardioprotective genes.…”

Section: Discussionmentioning

confidence: 99%

“…The early protection wanes rapidly so that by 3 hours no protection 239 is seen. Evolution of a delayed protective effect follows, and is established at 12 to 24 hours (1,20,21,43). After 96 hours no protection is observed.…”

Section: Introductionmentioning

confidence: 97%

Repeated Simulated Ischemia and Protection Against Gap Junctional Uncoupling

Sundset

Ytrehus

Zhang

et al. 2007

Cell Communication & Adhesion

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Ischemic preconditioning increases the heart's tolerance to a subsequent longer ischemic period. The aim of this study was to investigate the effect of early and delayed preconditioning on gap junction communication, connexin abundance, and phosphorylation in cultured neonatal rat cardiac myocytes. Prolonged ischemia followed 5 minutes after preconditioning in the early protocol, whereas 20 hours separated preconditioning and prolonged ischemia in the delayed preconditioning protocol. Gap junctional intercellular communication (GJIC) was assessed by Lucifer yellow dye transfer. An initial reduction in communication in response to sublethal ischemia was observed. This may be one mechanism whereby neighboring cells are protected from damaging substances produced during the first phase of subsequent regional ischemia in early preconditioning protocols. With respect to delayed preconditioning, the transient decrease in GJIC disappeared prior to prolonged ischemia, indicating that other mechanisms are responsible for delayed protection. Both early and delayed preconditioning preserved intercellular coupling after prolonged ischemia and this correlated with presence of less connexin43 dephosphorylation assessed by immunoblot.

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Characterisation of the infarct-limiting effect of delayed preconditioning: timecourse and dose-dependency studies in rabbit myocardium

Cited by 179 publications

References 19 publications

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

Inducible Nitric Oxide Synthase Mediates Delayed Myocardial Protection Induced by Activation of Adenosine A ₁ Receptors

Repeated Simulated Ischemia and Protection Against Gap Junctional Uncoupling

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Characterisation of the infarct-limiting effect of delayed preconditioning: timecourse and dose-dependency studies in rabbit myocardium

Cited by 179 publications

References 19 publications

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

Inducible Nitric Oxide Synthase Mediates Delayed Myocardial Protection Induced by Activation of Adenosine A 1 Receptors

Repeated Simulated Ischemia and Protection Against Gap Junctional Uncoupling

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Inducible Nitric Oxide Synthase Mediates Delayed Myocardial Protection Induced by Activation of Adenosine A ₁ Receptors