Small Animal Model for Myocardial Infarction

Staab, Robert J.; Lynch, Vince; Lau‐Cam, Cesar A.; Barletta, Michael

doi:10.1002/jps.2600661036

Cited by 10 publications

(3 citation statements)

References 15 publications

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“…Preclinical models of MI prove to be important in investigating pathophysiological mechanisms and therapeutic strategies. Since 1970s, rat models have been established for experimental cardiac research, because of their physiological features similar to that of humans . Furthermore, compared to other animals such as dogs or cats, rat models of MI are with lower costs, easier manipulation, higher survival rate, richer availability and less ethical concerns .…”

Section: Discussionmentioning

confidence: 99%

Hypericin as a Marker for Determination of Myocardial Viability in a Rat Model of Myocardial Infarction

Jiang

et al. 2014

Photochem & Photobiology

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The aim of this study was to investigate the necrosis-avid agent hypericin as a potential indicator for determination of myocardial infarction (MI). Male Sprague-Dawley rats (n = 30) weighing 350 ± 20 g were subjected to acute reperfused MI. Animals were divided into four groups (n = 6), in which hypericin was intravenously injected at 0, 1, 2 and 5 mg kg(-1) respectively. One day after injection, rats were euthanized with their hearts excised for qualitative and quantitative studies by means of microscopic fluorescence examination to decide the dosage of hypericin. Another group was injected with hypericin at the decided dose and evaluated by fluorescence macroscopy in colocalization with triphenyltetrazoliumchloride (TTC) and histomorphology. Infarct-to-normal contrast ratio and relative infarct size were quantified. Hypericin-induced red fluorescence was significantly brighter in necrotic than in viable myocardium as proven by a six times higher mean fluorescence density. Mean MI area was 35.66 ± 22.88% by hypericin fluorescence and 32.73 ± 21.98% by TTC staining (R(2) = 0.9803). Global MI-volume was 34.56 ± 21.07% by hypericin and 35.11 ± 20.47% by TTC staining (R(2) = 0.9933). The results confirm that hypericin specifically labeled necrosis, and enhanced the imaging contrast between the infarcted and normal myocardium, suggesting its potential applications for the assessment of myocardial viability.

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Section: Discussionmentioning

confidence: 99%

Hypericin as a Marker for Determination of Myocardial Viability in a Rat Model of Myocardial Infarction

Jiang

et al. 2014

Photochem & Photobiology

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“…Rats are the most commonly used laboratory animal for assessing ischemia-reperfusion injury in experiments. They are used to study the mechanisms of post-infarction pathology and to develop approaches reducing adverse cardiac events following ischemia-reperfusion injury in the myocardium [5][6][7]. In addition to experimental studies, an anatomically accurate computer modeling of the heart has become a valuable process for investigations of cardiac arrhythmia mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Anatomical Model of Rat Ventricles to Study Cardiac Arrhythmias under Infarction Injury

et al. 2021

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Species-specific computer models of the heart are a novel powerful tool in studies of life-threatening cardiac arrhythmias. Here, we develop such a model aimed at studying infarction injury in a rat heart, the most common experimental system to investigate the effects of myocardial damage. We updated the Gattoni2016 cellular ionic model by fitting its parameters to experimental data using a population modeling approach. Using four selected cellular models, we studied 2D spiral wave dynamics and found that they include meandering and break-up. Then, using an anatomically realistic ventricular geometry and fiber orientation in the rat heart, we built a model with a post-infarction scar to study the electrophysiological effects of myocardial damage. A post-infarction scar was simulated as an inexcitable obstacle surrounded by a border zone with modified cardiomyocyte properties. For cellular models, we studied the rotation of scroll waves and found that, depending on the model, we can observe different types of dynamics: anchoring, self-termination or stable rotation of the scroll wave. The observed arrhythmia characteristics coincide with those measured in the experiment. The developed model can be used to study arrhythmia in rat hearts with myocardial damage from ischemia reperfusion and to examine the possible arrhythmogenic effects of various experimental interventions.

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“…Myocardial infarct size, measured by excision and weighing of the damaged tissue, correlated well with the extent of the release of myocardial creatine phosphokinase (4,5). This enzyme offered many advantages over the other myocardial enzymes since it rose first following an infarction and returned to normal levels in approximately 3 days (6).…”

Section: Introductionmentioning

confidence: 99%

Effects of Pharmacological Intervention on Infarct Size following induced Myocardial Infarction in Rats

Barletta

Staab

Cam

et al. 1978

Journal of Pharmaceutical Sciences

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Small Animal Model for Myocardial Infarction

Cited by 10 publications

References 15 publications

Hypericin as a Marker for Determination of Myocardial Viability in a Rat Model of Myocardial Infarction

Hypericin as a Marker for Determination of Myocardial Viability in a Rat Model of Myocardial Infarction

Anatomical Model of Rat Ventricles to Study Cardiac Arrhythmias under Infarction Injury

Effects of Pharmacological Intervention on Infarct Size following induced Myocardial Infarction in Rats

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