Models for the study of arrhythmias in myocardial ischaemia and infarction: the use of the rat

Curtis, Michael J.; MacLeod, Bernard A.; Walker, Michael J.

doi:10.1016/s0022-2828(87)80585-0

Cited by 153 publications

(75 citation statements)

References 112 publications

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“…During ischemia, arrhythmias may develop, ranging in severity from isolated ventricular premature beats, through runs of ventricular tachycardia, to ventricular fibrillation (Tennant and Wiggers, 1935;Curtis et al, 1987;Carmeliet, 1999). Early arrhythmias (phase I arrhythmias) after coronary artery occlusion may contribute to sudden cardiac death following coronary occlusion (Janse and Wit, 1989).…”

Section: Contractile Dysfunction and Ventricular Arrhythmiasmentioning

confidence: 99%

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

Ferdinándy¹,

Schulz²,

Baxter³

2007

Pharmacol Rev

652

615

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Section: Contractile Dysfunction and Ventricular Arrhythmiasmentioning

confidence: 99%

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

Ferdinándy¹,

Schulz²,

Baxter³

2007

Pharmacol Rev

652

615

View full text Add to dashboard Cite

“…On the basis of previous experiences (31,34,35), the homogeneity in the experimental groups was guaranteed by adopting the two following inclusion criteria: (a) severity score of ventricular arrhythmias occurring 5-20 min after coronary occlusion within the score rank 3 and (b) the development of Low-T3S 24 h after I/R (I/R-L group).…”

Section: Inclusion Criteriamentioning

confidence: 99%

Early and Short-term Triiodothyronine Supplementation Prevents Adverse Postischemic Cardiac Remodeling: Role of Transforming Growth Factor-β1 and Antifibrotic miRNA Signaling

Nicolini

Forini

Kusmic

et al. 2015

Mol Med

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Activation of transforming growth factor (TGF)-β1 signaling in the ischemia/reperfusion (I/R) injured myocardium leads to dysregulation of miR-29-30-133, favoring the profibrotic process that leads to adverse cardiac remodeling (CR). We have previously shown that timely correction of the postischemic low-T3 syndrome (Low-T3S) exerts antifibrotic effects, but the underlying molecular players are still unknown. Here we hypothesize that a prompt, short-term infusion of T3 in a rat model of post I/R Low-T3S could hamper the early activation of the TGFβ1-dependent profibrotic cascade to confer long-lasting cardioprotection against adverse CR. Twenty-four hours after I/R, rats that developed the Low-T3S were randomly assigned to receive a 48-h infusion of 6 μg/kg/d T3 (I/R-L+T3) or saline (I/R-L) and sacrificed at 3 or 14 d post-I/R. Three days post-I/R, Low-T3S correction favored functional cardiac recovery. This effect was paralleled by a drop in TGFβ1 and increased miR-133a, miR-30c and miR-29c in the infarcted myocardium. Consistently, connective transforming growth factor (CTGF) and matrix metalloproteinase-2 (MMP-2), validated targets of the above miRNAs, were significantly reduced. Fourteen days post-I/R, the I/R-L+T3 rats presented a significant reduction of scar size with a better preservation of cardiac performance and LV chamber geometry. At this time, TGFβ1 and miR-29c levels were in the normal range in both groups, whereas miR-30c-133a, MMP-2 and CTGF remained significantly altered in the I/R group. In conclusion, the antifibrotic effect exerted by T3 in the early phase of postischemic wound healing triggers a persistent cardioprotective response that hampers the progression of heart dysfunction and adverse CR.

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“…The clinical relevance of systemic hypertension and cardiac hypertrophy has not yet been established in rat models because the ECG manifestations are unusual. 44 However, an extensive database of rat arrhythmias based on their widespread use for assessing various cardiovascular diseases and drug effects supports the notion that the advantages of using the rat as a model outweigh the disadvantages. Second, the IF-used in this study is not relevant to the clinical setting.…”

Section: Discussionmentioning

confidence: 99%

Arrhythmogenic and Inotropic Effects of Interferon Investigated in Perfused and in Vivo Rat Hearts. Influences of Cardiac Hypertrophy and Isoproterenol.

Odashiro

Hiramatsu

Yanagi

et al. 2002

Circ J

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Models for the study of arrhythmias in myocardial ischaemia and infarction: the use of the rat

Cited by 153 publications

References 112 publications

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

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

Early and Short-term Triiodothyronine Supplementation Prevents Adverse Postischemic Cardiac Remodeling: Role of Transforming Growth Factor-β1 and Antifibrotic miRNA Signaling

Arrhythmogenic and Inotropic Effects of Interferon Investigated in Perfused and in Vivo Rat Hearts. Influences of Cardiac Hypertrophy and Isoproterenol.

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