Characterisation and validation of a murine model of global ischaemia-reperfusion injury

Sumeray, Mark; Yellon, Derek M.

doi:10.1007/978-1-4615-4979-6_8

Cited by 26 publications

(33 citation statements)

References 7 publications

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“…Aging is associated with an increase in myocardial susceptibility to ischemia and a decrease in postischemic recovery of cardiac function [33]. Understanding the potential mechanisms of aging could lead to improved medical treatment of this increasing patient population.…”

Section: Discussionmentioning

confidence: 99%

Nitrative thioredoxin inactivation as a cause of enhanced myocardial ischemia/reperfusion injury in the aging heart

Zhang

Tao

Jiao

et al. 2007

Free Radical Biology and Medicine

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Objective-Several recent studies have demonstrated that thioredoxin (Trx) is an important antiapoptotic/cytoprotective molecule. The present study was designed to determine whether Trx activity is altered in the aging heart in a way that may contribute to increased susceptibility to myocardial ischemia/reperfusion (MI/R).Methods and Results-Compared to young animals, MI/R-induced cardiomyocyte apoptosis and infarct size were increased in aging animals (P<0.01). Trx activity was decreased in the aging heart before MI/R, and this difference was further amplified after MI/R. Trx expression was moderately increased and Trx nitration, a post-translational modification that inhibits Trx activity, was increased in the aging heart. Moreover, Trx-ASK1 complex formation was reduced and activity of p38 MAPK was increased. Treatment with FP15 (a peroxynitrite decomposition catalyst) reduced Trx nitration, increased Trx activity, restored Trx-ASK1 interaction, reduced P38 MAPK activity, attenuated caspase 3 activation and reduced infarct size in aging animals (p<0.01). Conclusions-Our results demonstrated that Trx activity is decreased in the aging heart by posttranslational nitrative modification. Interventions that restore Trx activity in the aging heart may be novel therapies to attenuate MI/R injury in aging patients.

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Section: Discussionmentioning

confidence: 99%

Nitrative thioredoxin inactivation as a cause of enhanced myocardial ischemia/reperfusion injury in the aging heart

Zhang

Tao

Jiao

et al. 2007

Free Radical Biology and Medicine

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“…Sumeray & Yellon (1 998) report -1 0 % infarction after 20 min ischaemia while others report 2545 %U (Marber et al 1995;Xi et al 1998) and up to 60% infarction (Morrison et al 2000). Ischaemia for 30 min results in as little as 8 O/o ( Yoshida et al 1996) or 25% (Yoshida et al 2000) to as much as 60'% infarction (Sumeray & Yellon, 1998). Others report 45-55% infarct development after 50min ischaemia (Li et al 1997;Kang et al 1999).…”

Section: Responses To Ischaemia-reperfusion: Isovolumic Contraction Vmentioning

confidence: 99%

“…Owing to a general paucity of background information, and the technical challenge of assessing contractile function via intraventricular balloon in small hearts, the majority of studies of ischaemia-reperfusion in mouse have been undertaken in unloaded empty hearts with function assessed via apicobasal displacement (Marber et al 1995;Plumier et al 1995;Yoshida et al 1996Yoshida et al ,2000Li et al 1997;Matherne et al 1997;Sumeray & Yellon 1998;Xi et al 1998;Kang et al 1999;Morrison et al 2000;Sumeray et al 2000). Fewer studies have been performed in isovolumically contracting hearts (Galinanes & Hearse, 1990;Chen et al 1998;Flogel et al 1999;Headrick et al 2000a;Zhao et a1.…”

Section: Responses To Ischaemia-reperfusion: Isovolumic Contraction Vmentioning

confidence: 99%

“…In terms of ischaemia and reperfusion, excessively variable responses have also been reported in different murine preparations (Galinanes & Hearse, 1990;Marber et al 1995;Plumier et al 1995;Radford et al 1996;Li et al 1997;Sumeray & Yellon, 1998;Xi et al 1998;Flogel et al 1999;Kang et al 1999;Headrick et al 2000a;Sumeray et al 2000;Yoshida et al 2000;Zhao et al 2000). Only one group has attempted to characterise the effects of ischaemia, and the relation between ischaemic duration and tissue injury, in the mouse heart (Sumeray & Yellon, 1998).…”

mentioning

confidence: 99%

“…Only one group has attempted to characterise the effects of ischaemia, and the relation between ischaemic duration and tissue injury, in the mouse heart (Sumeray & Yellon, 1998). It is unfortunate that these investigators employed unloaded empty hearts with…”

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confidence: 99%

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Functional properties and responses to ischaemia‐reperfusion in Langendorff perfused mouse heart

Headrick¹,

Peart²,

Hack³

et al. 2001

Experimental Physiology

112

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Despite minimal model characterisation Langendorff perfused murine hearts are increasingly employed in cardiovascular research, and particularly in studies of myocardial ischaemia and reperfusion. Reported contractility remains poor and ischaemic recoveries variable. We characterised function in C57/BL6 mouse hearts using a ventricular balloon or apicobasal displacement and assessed responses to 10-30 min global ischaemia. We examined the functional effects of pacing, ventricular balloon design, perfusate filtration, [Ca"] and temperature. Contractility was high in isovolumically functioning mouse hearts (measured as the change in pressure with time (+dP/dt), 6000-7000 mmHg s-I) and was optimal at a heart rate of -420 beats min-', with the vasculature sub-maximally dilated, and the cellular energy state high. Post-ischaemic recovery (after 40 min reperfusion) was related to the ischaemic duration: developed pressure recovered by 82 f YO, 73 f 4u/, 68 f 3%, 57 f 2% and 41 f 5% after 10, 15, 20, 25 and 30 min ischaemia, respectively. Ventricular compliance and elastance were both reduced post-ischaemia. Post-ischaemic recoveries were lower in the apicobasal model (80 +-4 YO, 58 k 7 YO, 40 +-3 %, 32 +-7 % and 25 2 5 YO) despite greater reflow and lower metabolic rate (pre-ischaemic myocardial O2 consumption (Vo2,,,,) 127 f 15 vs. 198 k 17 p l O2 min-' g-'), contracture, enzyme and purine efflux. Electrical pacing slowed recovery in both models, small ventricular balloons (unpressurised volumes C 50-60 p1) artificially depressed ventricular function and recovery from ischaemia, and failure to filter the perfusion fluid to C 0.45 pm depressed pre-and post-ischaemic function. With attention to these various experimental factors, the buffer perfused isovolumically contracting mouse heart is shown to be stable and highly energised, and to possess a high level of contractility, The isovolumic model is more reliable in assessing ischaemic responses than the commonly employed apicobasal model. Experimental Physiology (200 1) 86.6, 703-7 16.

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Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection

et al. 2018

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Characterisation and validation of a murine model of global ischaemia-reperfusion injury

Cited by 26 publications

References 7 publications

Nitrative thioredoxin inactivation as a cause of enhanced myocardial ischemia/reperfusion injury in the aging heart

Nitrative thioredoxin inactivation as a cause of enhanced myocardial ischemia/reperfusion injury in the aging heart

Functional properties and responses to ischaemia‐reperfusion in Langendorff perfused mouse heart

Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection

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