Myocardial infarct size—Limiting effect of ischemic preconditioning: Its natural decay and the effect of repetitive preconditioning

Miura, Tetsuji; Adachi, Takeo; Ogawa, Takashi; Iwamoto, Toshihiro; Tsuchida, Akihito; Iimur, Osamu

doi:10.1016/1054-8807(92)90018-j

Cited by 37 publications

(10 citation statements)

References 13 publications

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“…16,17 Similarly, we have shown that in immature rabbit hearts preconditioned by a single 5-minute period of occlusion, the memory of preconditioning is also lost after a time delay of 30 minutes between the preconditioning stimulus and the prolonged ischemic insult. Our data suggest there is no age-related difference in the memory of preconditioning between immature and mature rabbit hearts.…”

Section: Memory Of Preconditioningmentioning

confidence: 91%

“…The duration of this period determines whether the myocardium retains the memory of the preconditioning stimulus that confers protection during subsequent sustained ischemia. 16,17 We performed the following experiments in random order using 10 hearts from 4 groups. The 4 experimental groups were as follows: group 7, nonpreconditioned; group 8, 1ϫ5 minutes of preconditioning with 10 minutes of reperfusion; group 9, 1ϫ5 minutes of preconditioning with 20 minutes of reperfusion; and group 10, 1ϫ5 minutes of preconditioning with 30 minutes of reperfusion.…”

Section: Memory Studiesmentioning

confidence: 99%

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Preconditioning in Immature Rabbit Hearts

1999

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Section: Memory Of Preconditioningmentioning

confidence: 91%

Section: Memory Studiesmentioning

confidence: 99%

Preconditioning in Immature Rabbit Hearts

1999

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“…After the seminal definition of preconditioning, a large number of studies described the natural history of this phenomenon. It has been shown that protection wanes and is eventually lost when multiple cycles of preconditioning are applied before the sustained ischemia (Cohen et al ., 1994; Iliodromitis et al ., 1997) or when the time interval between short and long ischemia is very prolonged (Van Winkle et al ., 1991; Miura et al ., 1992).…”

Section: Discussionmentioning

confidence: 99%

Oral nicorandil recaptures the waned protection from preconditioning in vivo

Iliodromitis

Cokkinos

Ζώγα

et al. 2003

British J Pharmacology

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1 Protection from preconditioning (PC) wanes and is eventually lost when multiple bouts of short ischemia or a prolonged reperfusion interval precedes the following sustained ischemia. The activation of mitochondrial K ATP channels plays a pivotal role in the intracellular signaling of PC. We tested whether the K ATP channel opener nicorandil (nic) preserves the given protection from PC in conditions where this benefit decays and is lost. 2 Eight groups of rabbits were divided into two equal series of experiments, one without nic (placebo) and one with nic treatment. Nic was given orally for 5 consecutive days in a dose of 5 mg kg À1 d À1 . In a second step, four additional groups were treated with nic plus the K ATP channel blocker 5HD and 1 additional control group with nitroglycerin only. All the animals were anesthetized and then subjected to 30 min of myocardial ischemia and 2 h of reperfusion with one of the following interventions before the sustained ischemia: Control groups to no intervention; 3PC groups to three cycles of 5-min ischemia-10-min reperfusion; 8PC groups to eight cycles of 5-min ischemia -10-min reperfusion; and 3PC90 groups to the same interventions as the 3PC groups but with a prolonged (90 min) intervening reperfusion interval before the sustained ischemia. The infarcted and the risk areas were expressed in percent. 3 There was no significant change in infarct size between the placebo, the nic and the 5HD-nic in the control groups (41.574.7, 43.977.1 and 48.776.4%) and 3PC groups (10.373.4, 12.273.9 and 12.674.5%). However, there was a significant decrease after nic treatment in groups 8PC (47.778.8% vs 13.072.6%, Po0.01) and 3PC90 (37.376.0% vs 14.272.4%, Po0.01), which was abrogated (38.274.7 and 42.774.4%, respectively, for 8PC and 3PC90 groups). Nitroglycerin had no effect on infarct size (39.173.1%, P ¼ NS vs other controls). 4 Oral treatment with nic recaptures the waned protection of PC, both after repetitive bouts of short ischemia or after a prolonged reperfusion interval, preserving the initially obtained benefit. Nic by itself is insufficient to initiate PC in vivo.

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“…References single cycle is sufficient to impart marked protection in the in vivo rabbit (16), and two cycles induce a maximal cardioprotective effect (7). Nonetheless, it is impossible to exclude the chance that remote PC might have been achieved with more than 2 cycles of PC.…”

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confidence: 99%

Preconditioning one myocardial region does not neccessarily precondition the whole rabbit heart

Nakano

Heusch

Cohen

et al. 2002

Basic Research in Cardiology

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A previous study in dogs indicated that preconditioning (PC) of a specific myocardial region not only evoked a local cardioprotective effect but also rendered remote myocardium resistant to infarction. In the present study we devised a method to test for remote PC in the rabbit which it is not possible to ligate two separate coronary branches on the same heart. In situ hearts were subjected to PC with two cycles of 5-min regional ischemia/5-min reperfusion. Following this in vivo PC protocol, the hearts were removed and perfused on a Langendorff apparatus with crystalloid buffer. They then underwent 30 min of global ischemia with the entire left ventricle at risk followed by 2 h of reperfusion. At the end of the experiment the myocardium previously subjected to the in vivo PC protocol (preconditioned region) was identified as the tissue without fluorescence after fluorescent particles had been injected into the aortic root following reocclusion of the snared branch of the left coronary artery. Infarcted myocardium was identified by triphenyltetrazolium chloride staining. Tissue salvage was observed only in the preconditioned region where 13.2 +/- 3.6% of the myocardium infarcted as opposed to 44.6 +/- 1.3% in the remaining non-preconditioned left ventricular tissue (p < 0.05, n = 6). In sham-operated hearts (snare but no PC), infarction was similar in both the snared vessel's perfusion territory and the rest of the left ventricular myocardium (49.2 +/- 6.5% vs. 43.7 +/- 3.7%, n = 5). Hence PC of one myocardial region does not necessarily confer PC protection to all regions of the heart. Because remote PC could not be demonstrated in rabbits, this phenomenon may be species or protocol-specific, and should not be assumed to occur in man.

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Myocardial infarct size—Limiting effect of ischemic preconditioning: Its natural decay and the effect of repetitive preconditioning

Cited by 37 publications

References 13 publications

Preconditioning in Immature Rabbit Hearts

Preconditioning in Immature Rabbit Hearts

Oral nicorandil recaptures the waned protection from preconditioning in vivo

Preconditioning one myocardial region does not neccessarily precondition the whole rabbit heart

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