Ischaemic pre‐conditioning means an increased adenosine metabolism with decreased glycolytic flow in ischaemic pig myocardium

Åberg, Anna-Maja; Ahlström, Katarina; Abrahamsson, Pernilla; Waldenström, Anders; Ronquist, Gunnar; Hauck, Philip; Johansson, Gillis; Biber, Björn; Haney, Michael

doi:10.1111/j.1399-6576.2010.02312.x

Cited by 3 publications

(2 citation statements)

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“…, 1998). At some point during an ischaemic period, the myocardial glycogen stores can no longer be exploited, and then this energy pathway contributes no further (Åberg et al. , 2010).…”

Section: Introductionmentioning

confidence: 99%

Ischaemic preconditioning reduces myocardial calcium overload in coronary‐occluded pig hearts shown by continuous in vivo assessment using microdialysis

Waldenström

Ronquist

Åberg

et al. 2011

Clin Physio Funct Imaging

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During ischaemia, ATP depletion leads to insufficient fuelling for Na(+) /K(+) ATPase, decreased electrochemical potential and increased influx of calcium ions. This study demonstrated a means to assess the effects of ischaemic preconditioning (IP) on the free intracellular Ca(2+) pool during prolonged ischaemia. In a porcine myocardial ischaemia model, microdialysis (MD) was used for sampling of metabolic and injury markers in IP and non-IP (control) groups. (45) Ca(2+) was delivered in microperfusate locally to ischaemic myocardium, with distribution and uptake assessed by (45) Ca(2+) recovery in microdialysate. Cardiomyocytes in vitro were exposed to a Ca(2+) ionophore and tested for (45) Ca(2+) uptake. An accentuated myocardial calcium ion influx (observed as an increased microdialysate (45) Ca(2+) recovery in the extracellular milieu) was noted in control pigs compared with IP pigs during ischaemia. Suspended cardiomyocytes preincubated with a Ca(2+) ionophore to increase the intracellular calcium ion pool and subsequently incubated with (45) Ca(2+) , displayed lower (45) Ca(2+) uptake in cells compared with control cells not exposed to the ionophore, corroborating the idea of a strong relationship between degree of intracellular calcium overload and microdialysate (45) Ca(2+) recovery. The ischaemic insult was differentially verified by metabolic and injury markers. We introduce an in vivo method for serial assessment of myocardial calcium overload during ischaemia, using a MD technique and (45) Ca(2+) inclusion. IP leads to relatively less calcium overload as assessed by this new method, and we interpret this to mean that reduction in calcium overload is an important part of the IP protective effect.

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“…, 1998). At some point during an ischaemic period, the myocardial glycogen stores can no longer be exploited, and then this energy pathway contributes no further (Åberg et al. , 2010).…”

Section: Introductionmentioning

confidence: 99%

Ischaemic preconditioning reduces myocardial calcium overload in coronary‐occluded pig hearts shown by continuous in vivo assessment using microdialysis

Waldenström

Ronquist

Åberg

et al. 2011

Clin Physio Funct Imaging

View full text Add to dashboard Cite

show abstract

“…Adenosine can act as a neuromodulator, as a modulator of vasomotor tone, notably of the autoregulation of retinal arterioles, and as an activator of ionic channels in the membrane of mitochondria. [30][31][32] Further, A1 receptor activation has been considered important in RIPinduced protection of the myocardium 33 ; adenosine turnover has been reported to be upregulated in myocardium by direct ischemia, 34 and adenosine infusion in perfused cat eyes resulted in supernormal b-waves and vasodilation. 18,35 Adenosine is then a candidate mediator for the effect reported here, the RIP-induced supernormality of the a-and b-waves; to test this, further investigation is required.…”

Section: Possible Mechanismsmentioning

confidence: 99%