Ischemic preconditioning preserves creatine phosphate and intracellular pH.

Kida, Mitsugu; Fujiwara, Hisayoshi; Ishida, Moriharu; Kawai, Chuichi; Ohura, M.; Miura, Iwao; Yabuuchi, Youichi

doi:10.1161/01.cir.84.6.2495

Cited by 174 publications

(57 citation statements)

References 28 publications

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“…119,120 Because the duration of protection by preconditioning is also related to the time course of postischemic glycogen recovery, 121 the data, when taken together, show that protection by ischemic preconditioning reduces glycogen breakdown, therefore attenuating the accumulation of metabolic end products and the development of intracellular acidosis. The slower decline of both pH i and highenergy phosphates in preconditioned hearts during no-flow ischemia 122 is in agreement with this hypothesis. Most of the preconditioning protocols are performed on models of noflow ischemia; this further illustrates the importance of limiting the accumulation of glycolytic end products in the absence of residual coronary flow.…”

Section: Glycogen and Ischemic Preconditioningsupporting

confidence: 86%

Glucose for the Heart

Depré¹,

Vanoverschelde²,

Taegtmeyer³

1999

Circulation

377

260

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Section: Glycogen and Ischemic Preconditioningsupporting

confidence: 86%

Glucose for the Heart

Depré¹,

Vanoverschelde²,

Taegtmeyer³

1999

Circulation

377

260

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“…In spite of much research, the mechanism(s) underlying the phenomenon of preconditioning are not fully defined. A number of investigators have found that ATP content falls only during the first occlusion (32)(33)(34). Since a significant fall in pHi can occur within the first few minutes of occlusion ( 13), we speculate that acidosis attenuates adenine nucleotide degradation and adenosine production in subsequent periods of ischemia (long or short) because 5'-NT activity is inhibited.…”

Section: Inhibitors Of5'-nt In Vivomentioning

confidence: 73%

Acidosis during ischemia promotes adenosine triphosphate resynthesis in postischemic rat heart. In vivo regulation of 5'-nucleotidase.

Bak¹,

Ingwall²

1994

J. Clin. Invest.

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Capacity for ATP resynthesis during recovery from ischemia or hypoxia is limited to the size of the adenine nucleotide pool. which is determined in part by the activity ofcytosolic 5'-nucleotidase (5'-NT): AMP -* adenosine plus inorganic phosphate (Pi). To define in vivo regulation of 5'-NT, we used the tools of 31P nuclear magnetic resonance (NMR) spectroscopy and chemical assay to measure the substrates (AMP), products (Pi, adenosine, and its catabolites), and inhibitors (Pi and H+) of 5'-NT in isolated perfused rat hearts exposed to hypoxia (where pH remains near 7) and no flow, global ischemia (where pH falls to 6.1). We estimated 5'-NT reaction velocity, assessed the relative contributions of Pi and H+ to enzyme inhibition, and defined the consequences of changes in 5'-NT activity on ATP resynthesis after hypoxia and ischemia. We conclude that (a) 5'-NT is activated during hypoxia and early ischemia but is inhibited during prolonged ischemia, (b) H' (pH < 6.2) is a potent inhibitor of 5'-NT, and (c) differences in AMP accumulation are sufficient to explain the differences in the capacity for net ATP resynthesis in ischemic and hypoxic tissue. These observations have implications for our understanding of heterogeneity of ischemic injury and myocardial protection during ischemia. (J. Clin. Invest. 1994. 93:40-49.)

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“…[18][19][20] Forbes et al indicated that DZ 6 as well as IPC 12 reduced the decrease in pHi during ischemia. Our data showed that although IPC attenuated ischemic acidification, DZ did not affect the degree of ischemic acidification.…”

Section: Ipc and Intracellular Ph During Ischemiamentioning

confidence: 99%

“…IPC also has beneficial effects on energy metabolism, such as reduced intracellular acidification during ischemia and postischemic preservation of high-energy phosphates. [18][19][20] Measurement of these parameters may reveal the difference in the cardioprotective mechanisms between IPC and DZ. Moreover, a comparison of IPC and DZ under the same experimental condition would minimize the discrepancy in the results caused by the experimental conditions and models used.…”

mentioning

confidence: 99%

Difference in the Cardioprotective Mechanisms Between Ischemic Preconditioning and Pharmacological Preconditioning by Diazoxide in Rat Hearts

Wakahara¹,

Katoh²,

Yaguchi³

et al. 2004

Circ J

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schemic preconditioning (IPC) is a phenomenon whereby brief intermittent periods of ischemia protect the myocardium against subsequent lethal ischemia. 1 Although the mechanisms responsible for IPC still remain elusive, several factors, such as adenosine, acetylcholine and opioids, which activate protein kinase C, have been implicated in the cardioprotective effect of IPC. 2 Recently, ATP-sensitive potassium (KATP) channels and reactive oxygen species (ROS), among the signaling pathways mediating IPC, have attracted considerable attention. Though the involvement of sarcolemmal KATP channels in IPC was first suggested, 3 subsequent studies have reported that mitochondrial KATP (mitoKATP) channels play a potential role for the cardioprotective effects of KATP channel openers. 4 More recent studies have indicated that the opening of mitoKATP channels induces cardioprotection by generating ROS, which may act as intracellular messengers. 5,6 It has been reported that pretreatment with mitoKATP channel openers 4 or exogenous H2O2 7,8 induces IPC-like protective effects, and that IPC-induced cardioprotection is antagonized by mitoKATP channel inhibitors 9,10 or ROS scavengers. 11,12 These findings support the hypothesis that IPC is mediated through the opening of mitoKATP channels and ROS production. Nevertheless, several investigators have argued against the contribution of mitoKATP channels [13][14][15]17 to IPC. The protective effects of IPC and the mitoKATP channel opener diazoxide (DZ) in whole heart models have been generally evaluated as reduced infarct size and improved contractile function during reperfusion. IPC also has beneficial effects on energy metabolism, such as reduced intracellular acidification during ischemia and postischemic preservation of high-energy phosphates. [18][19][20] Measurement of these parameters may reveal the difference in the cardioprotective mechanisms between IPC and DZ. Moreover, a comparison of IPC and DZ under the same experimental condition would minimize the discrepancy in the results caused by the experimental conditions and models used. However, few studies have compared the effects of IPC and DZ on energy metabolism under the same experimental conditions. Therefore, in the present study we investigated the involvement of the opening of mitoKATP channels and ROS production in IPC-and DZ-induced cardioprotection, using the mitoKATP channel inhibitor 5-hydroxydecanoate (5-HD) and the antioxidant N-acetylcysteine (NAC), in perfused Background Recent studies have implicated the opening of mitochondrial KATP (mitoKATP) channels and the production of reactive oxygen species (ROS) in the cardioprotective mechanism of ischemic preconditioning (IPC). Methods and ResultsThe involvement of mitoKATP channels and ROS in the cardioprotective effects of both IPC and the mitoKATP channel opener diazoxide (DZ) was investigated in ischemic/reperfused rat hearts. The effects of IPC and DZ on myocardial high-energy phosphate concentrations and intracellular pH (pHi) were also examined using 31...

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Ischemic preconditioning preserves creatine phosphate and intracellular pH.

Cited by 174 publications

References 28 publications

Glucose for the Heart

Glucose for the Heart

Acidosis during ischemia promotes adenosine triphosphate resynthesis in postischemic rat heart. In vivo regulation of 5'-nucleotidase.

Difference in the Cardioprotective Mechanisms Between Ischemic Preconditioning and Pharmacological Preconditioning by Diazoxide in Rat Hearts

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