Does the Antiarrhythmic Effect of Ischemie Preconditioning in Rats Involve the L-Arginine Nitric Oxide Pathway?

Lu, Hua-Rong; Remeysen, Paul; F, De Clerck

doi:10.1097/00005344-199504000-00003

Cited by 44 publications

(21 citation statements)

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“…The importance of NO in the conventional no-flow ischaemia-induced preconditioning is controversial (Vegh et al 1992;Weselcouch et al 1995;Lu et al 1995), however, our previous studies support a role of the NO-cGMP system in pacing-induced preconditioning in rabbits and rats (Ferdinandy et al 1996;Szilvassy et al 1994a, b). The discrepancy may be explained by the different biochemical mechanisms in no-flow ischaemia-induced preconditioning and that induced by rapid pacing (Ferdinandy et al 1995b).…”

Section: No and Preconditioningmentioning

confidence: 78%

“…The role of NO in the mechanism of preconditioning is controversial. Vegh et al (1992) found that the antiarrhythmic effect of preconditioning induced by short periods of coronary occlusion was abolished by administration of N Gnitro-L-arginine methyl ester in anaesthetized dogs; Lu et al (1995) and Weselcouch and associates (1995) could not confirm these results in anaesthetized rats and in isolated rat hearts. However, these studies focused on the antiarrhythmic effect of preconditioning induced by 'no-flow' ischaemia, and no direct measurement of myocardial NO was attempted.…”

Section: Introductionmentioning

confidence: 95%

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Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: role of nitric oxide and CGRP?

Ferdinándy

Csont

Csonka

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

100

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Section: No and Preconditioningmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 95%

Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: role of nitric oxide and CGRP?

Ferdinándy

Csont

Csonka

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

100

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“…34 Our present results support those of Vegh at al, 11 who demonstrated that 10 mg/kg LNA methyl ester abolished the antiarrhythmic effect of preconditioning in a coronary occlusion model in anesthetized dogs. However, studies by Lu et al 35 using 10 mg/kg N G -monomethyl-L-arginine or LNA methyl ester in anesthetized rats with coronary occlusion/ reperfusion and by Weselcouch et al 30 using 30 mol/L LNA methyl ester in isolated rat hearts showed, surprisingly, that the different NOS inhibitors did not interfere with the outcome of ischemia/reperfusion with or without preceding preconditioning as assessed by postischemic myocardial function, LDH release, 30 and arrhythmias. 35 Because NO generation was not determined and only a single dose of NOS inhibitor was used in these studies, it is difficult to interpret these negative results.…”

Section: No and Preconditioningmentioning

confidence: 95%

Classic Preconditioning Decreases the Harmful Accumulation of Nitric Oxide During Ischemia and Reperfusion in Rat Hearts

et al. 1999

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Background-The role of NO in the mechanism of preconditioning is not understood. Therefore, we studied the effect of preconditioning and subsequent ischemia/reperfusion on myocardial NO content in the presence of an NO synthase (NOS) inhibitor. Methods and Results-Isolated working rat hearts were subjected to preconditioning protocols of 3 intermittent periods of rapid pacing or no-flow ischemia of 5 minutes' duration each followed by a test 30 minutes of global no-flow ischemia and 15 minutes of reperfusion. Test ischemia/reperfusion resulted in a deterioration of myocardial function and a considerable increase in cardiac NO content as assessed by electron spin resonance. Preconditioning improved postischemic myocardial function and markedly decreased test ischemia/reperfusion-induced NO accumulation. In the presence of 4.6 mol/L N G -nitro-L-arginine (LNA), basal cardiac NO content decreased significantly, although test ischemia/reperfusion-induced functional deterioration and NO accumulation were not affected in nonpreconditioned hearts. However, the protective effects of preconditioning on both test ischemia/reperfusion-induced functional depression and NO accumulation were abolished. When 4.6 mol/L LNA was administered after preconditioning, it failed to block the effect of preconditioning. In the presence of 46 mol/L LNA, ischemia/reperfusion-induced NO accumulation was significantly decreased and postischemic myocardial function was improved in nonpreconditioned hearts. Conclusions-Our results show that (1) although NO synthesis by the heart is necessary to trigger classic preconditioning, preconditioning in turn attenuates the accumulation of NO during ischemia/reperfusion, and (2)

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“…However, the requirement for RNS in the triggering of preconditioning is controversial, as some groups find evidence for the involvement of nitric oxide (NO) during the early window of protection (21,32) but others do not (27). In cardiomyocytes, inhibition of NO synthase (NOS) with N -nitro-L-arginine methyl ester (L-NAME) did not abolish the ROS signal during hypoxic triggering (42), which suggests that NO is not required for ROS generation during hypoxic triggering.…”

mentioning

confidence: 99%

ROS and NO trigger early preconditioning: relationship to mitochondrial K_ATP channel

Lebuffe

Schumacker

Shao

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

222

160

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NO trigger early preconditioning: relationship to mitochondrial K ATP channel. Am J Physiol Heart Circ Physiol 284: H299-H308, 2003. First published September 26, 2002 10.1152/ajpheart.00706.2002Reactive oxygen species (ROS) and nitric oxide (NO) are implicated in induction of ischemic preconditioning. However, the relationship between these oxidant signals and opening of the mitochondrial ATP-dependent potassium (K ATP) channel during early preconditioning is not fully understood. We observed preconditioning protection by hypoxia, exogenous H 2O2, or PKC activator PMA in cardiomyocytes subjected to 1-h ischemia and 3-h reperfusion. Protection was abolished by K ATP channel blocker 5-hydroxydecanoate (5-HD) in each case, indicating that these triggers must act upstream from the K ATP channel. Inhibitors of NO synthase abolished protection in preconditioned cells, suggesting that NO is also required for protection. DAF-2 fluorescence (NO sensitive) increased during hypoxic triggering. This was amplified by pinacidil and inhibited by 5-HD, indicating that NO is generated subsequent to K ATP channel activation. Exogenous NO during the triggering phase conferred protection blocked by 5-HD. Exogenous NO also restored protection abolished by 5-HD or N -nitro-L-arginine methyl ester in preconditioned cells. Antioxidants given during pinacidil or NO triggering abolished protection, confirming that ROS are generated by K ATP channel activation. Coadministration of H 2O2 and NO restored PMA-induced protection in 5-HD-treated cells, indicating that ROS and NO are required downstream from the K ATP channel. We conclude that ROS can trigger preconditioning by causing activation of the K ATP channel, which then induces generation of ROS and NO that are both required for preconditioning protection. hydrogen peroxide; nitric oxide; ischemia; cardiomyocytes PRECONDITIONING CONFERS PROTECTION against ischemiareperfusion injury in the heart. After a brief triggering stimulus is applied, the "early window" of protection begins within minutes and lasts for several hours. The persistence of protection after removal of the trigger indicates that a signal transduction pathway has been activated. Numerous triggers of preconditioning have been identified, including brief hypoxia/ischemia, opioids, ACh, bradykinin, activators of PKC, and pharmacological agents that activate the mitochondrial ATPdependent potassium (mitoK ATP ) channel (10,13,15,16,26,39,50). However, the signal transduction sequence activated by these triggers is not fully understood.Reactive oxygen species (ROS) have been implicated as participants in the signaling pathway involved in preconditioning triggering (1,2,4,23,41). We previously reported (42, 50) that exogenous H 2 O 2 induces preconditioning in cardiomyocytes and that mitochondrial ROS are involved in the triggering by hypoxia or by ACh administration. However, an interesting controversy has developed regarding the relationship between the mitoK ATP channel activation and the ROS signal during triggering. On...

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Does the Antiarrhythmic Effect of Ischemie Preconditioning in Rats Involve the L-Arginine Nitric Oxide Pathway?

Cited by 44 publications

References 0 publications

Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: role of nitric oxide and CGRP?

Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: role of nitric oxide and CGRP?

Classic Preconditioning Decreases the Harmful Accumulation of Nitric Oxide During Ischemia and Reperfusion in Rat Hearts

ROS and NO trigger early preconditioning: relationship to mitochondrial K_ATP channel

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Does the Antiarrhythmic Effect of Ischemie Preconditioning in Rats Involve the L-Arginine Nitric Oxide Pathway?

Cited by 44 publications

References 0 publications

Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: role of nitric oxide and CGRP?

Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: role of nitric oxide and CGRP?

Classic Preconditioning Decreases the Harmful Accumulation of Nitric Oxide During Ischemia and Reperfusion in Rat Hearts

ROS and NO trigger early preconditioning: relationship to mitochondrial KATP channel

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ROS and NO trigger early preconditioning: relationship to mitochondrial K_ATP channel