Ischaemic preconditioning by partial occlusion without intermittent reperfusion

Koning, M. M. G.; Simonis, Laurens A J; Zeeuw, Sandra de; Nieukoop, Selma; Post, S.; Verdouw, Pieter D.

doi:10.1093/cvr/28.8.1146

Cited by 40 publications

(11 citation statements)

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“…4, left), which is in line with previous observations that infarct size is not correlated with oxygen demand at the onset of occlusion (Miura et al, 1992;Koning et al, 1994;Gho et al, 1996;Van den Doel et al, 1998). In addition, the cardioprotection by BMOV administered before reperfusion was also not correlated with the rate-pressure product at the onset of reperfusion (Fig.…”

Section: Vanadate Attenuates Reperfusion Injurysupporting

confidence: 90%

The Tyrosine Phosphatase Inhibitor Bis(Maltolato)Oxovanadium Attenuates Myocardial Reperfusion Injury by Opening ATP-Sensitive Potassium Channels

Liem

Gho²,

Gho³

et al. 2004

J Pharmacol Exp Ther

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Vanadate has been shown to inhibit tyrosine phosphatase, leading to an increased tyrosine phosphorylation state. The latter has been demonstrated to be involved in the signal transduction pathway of ischemic preconditioning, the most potent endogenous mechanism to limit myocardial infarct size. Furthermore, there is evidence that phosphatase inhibition may be cardioprotective when given late after the onset of ischemia, but the mechanism of protection is unknown. We tested the hypothesis that the organic vanadate compound bis(maltolato)-oxovanadium (BMOV) limits myocardial infarct size by attenuating reperfusion injury and investigated the underlying mechanism. Myocardial infarction was produced in 112 anesthetized rats by a 60-min coronary artery occlusion, and infarct size was determined histochemically after 180 min of reperfusion. Intravenous infusion of BMOV in doses of 3.3, 7.5, and 15 mg/kg i.v. decreased infarct size dose-dependently from 70 Ϯ 2% of the area at risk in vehicle-treated rats down to 41 Ϯ 5% (P Ͻ 0.05 versus control), when administered before occlusion. Administration of the low dose just before reperfusion was ineffective, but administration of the higher doses was equally cardioprotective as compared with administration before occlusion. The cardioprotection by BMOV was abolished by the tyrosine kinase inhibitor genistein and by the ATP-sensitive potassium (K ϩ ATP ) channel blocker glibenclamide but was not affected by the ganglion blocker hexamethonium. We conclude that BMOV afforded significant cardioprotection principally by limiting reperfusion injury. The mode of action appears to be by opening of cardiac K ϩ ATP channels via increased tyrosine phosphorylation.

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Section: Vanadate Attenuates Reperfusion Injurysupporting

confidence: 90%

The Tyrosine Phosphatase Inhibitor Bis(Maltolato)Oxovanadium Attenuates Myocardial Reperfusion Injury by Opening ATP-Sensitive Potassium Channels

Liem

Gho²,

Gho³

et al. 2004

J Pharmacol Exp Ther

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“…A flow reduction to 30% of baseline for 30 min without intermittent reperfusion before 60 min of total coronary occlusion reduces infarct size in pigs (Koning et al, 1994); however, this effect is transmurally heterogeneous, insofar as the preconditioning ischemia reduces infarct size in the epicardium, but actually exacerbates infarction in the endocardium (Koning et al, 1995). Similarly, preconditioning without intermittent reperfusion before the index ischemia is seen when a 10-min coronary occlusion precedes 80 min of low-flow ischemia in pigs (Schulz et al, 1995a).…”

Section: Duration and Severity Of Ischemia And Reperfusion In Precondmentioning

confidence: 98%

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

Ferdinándy¹,

Schulz²,

Baxter³

2007

Pharmacol Rev

644

615

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“…19 After the heart was excised, the left ventricle was isolated and cut parallel to the atrioventricular groove into 5 slices of equal thickness. After the area at risk of each slice was demarcated on an acetate sheet under ultraviolet light, the slices were incubated in 0.125 g para-nitroblue tetrazolium (Sigma Chemical Co) per liter of phosphate buffer (pH 7.4) at 37°C for 30 minutes, and the nonstained pale infarcted area was also traced onto the sheet.…”

Section: Infarct Sizementioning

confidence: 99%

“…Myocardial infarct size was defined as the ratio of the summed infarct areas and summed areas at risk. 19 …”

Section: Infarct Sizementioning

confidence: 99%

Cardioprotection in Pigs by Exogenous Norepinephrine but not by Cerebral Ischemia–Induced Release of Endogenous Norepinephrine

Zeeuw

Lameris

Duncker

et al. 2001

Stroke

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Background and Purpose-Endogenous norepinephrine release induced by cerebral ischemia may lead to small areas of necrosis in normal hearts. Conversely, norepinephrine may be one of the mediators that limit myocardial infarct size by ischemic preconditioning. Because brief ischemia in kidneys or skeletal muscle limits infarct size produced by coronary artery occlusion, we investigated whether cardiac norepinephrine release during transient cerebral ischemia also elicits remote myocardial preconditioning. Methods-Forty-one crossbred pigs of either sex were assigned to 1 of 7 experimental groups, of which in 6 groups myocardial infarct size was determined after a 60-minute coronary occlusion and 120 minutes of reperfusion. One group served as control (no pretreatment), while the other groups were pretreated with either cerebral ischemia or an intracoronary infusion of norepinephrine. Results-In 10 anesthetized control pigs, infarct size was 84Ϯ3% (meanϮSEM) of the area at risk after a 60-minute coronary occlusion and 120 minutes of reperfusion. Intracoronary infusion of 0.03 nmol/kg · min Ϫ1 norepinephrine for 10 minutes before coronary occlusion did not affect infarct size (80Ϯ3%; nϭ6), whereas infusion of 0.12 nmol/kg · min Ϫ1 limited infarct size (65Ϯ2%; nϭ7; PϽ0.05). Neither 10-minute (nϭ5) nor 30-minute (nϭ6) cerebral ischemia produced by elevation of intracranial pressure before coronary occlusion affected infarct size (83Ϯ4% and 82Ϯ3%, respectively). Myocardial interstitial norepinephrine levels tripled during cerebral ischemia and during low-dose norepinephrine but increased 10-fold during high-dose norepinephrine. Norepinephrine levels increased progressively up to 500-fold in the area at risk during the 60-minute coronary occlusion, independent of the pretreatment, while norepinephrine levels remained unchanged in adjacent nonischemic myocardium and arterial plasma. Conclusions-Cerebral ischemia preceding a coronary occlusion did not modify infarct size, which is likely related to the modest increase in myocardial norepinephrine levels during cerebral ischemia. The infarct size limitation by high-dose exogenous norepinephrine is not associated with blunting of the ischemia-induced increase in myocardial interstitial norepinephrine levels. (Stroke. 2001;32:767-774.)

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Ischaemic preconditioning by partial occlusion without intermittent reperfusion

Abstract: Myocardium can be preconditioned with a flow reduction to 30% of baseline for 30 min without intermittent reperfusion (two stage Harris model). The positive intercept on the AR axis of the IS-AR relationship warrants caution of the use of IS/AR as an index for infarct size limitation.

Cited by 40 publications

References 0 publications

The Tyrosine Phosphatase Inhibitor Bis(Maltolato)Oxovanadium Attenuates Myocardial Reperfusion Injury by Opening ATP-Sensitive Potassium Channels

The Tyrosine Phosphatase Inhibitor Bis(Maltolato)Oxovanadium Attenuates Myocardial Reperfusion Injury by Opening ATP-Sensitive Potassium Channels

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

Cardioprotection in Pigs by Exogenous Norepinephrine but not by Cerebral Ischemia–Induced Release of Endogenous Norepinephrine

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