Key result
Peripheral ghrelin attenuates myocyte dysfunction and preserves atrial ultrastructure in a rat model of MI.
Why the study?
Does ghrelin improve atrial tissue ultrastructure in a rat model of experimentally-induced myocardial infarction?
Does ghrelin improve atrial tissue ultrastructure in a rat model of experimentally-induced myocardial infarction?
In a rat model of myocardial infarction, peripheral ghrelin administration protects atrial tissue ultrastructure and inhibits cardiomyocyte apoptosis.
Supports preclinical testing of ghrelin for post-MI atrial protection; leaves open clinical relevance.
Ghrelin is a novel growth hormone-releasing peptide administered to treat myocardial infarction (MI). However, the underlying mechanism of its protective effects against MI remains unclear. A total of sixty healthy Sprague Dawley male rats were included. The first one is the sham-operated control group were the rats that underwent the same surgical used to induce MI but without tying the left anterior descending coronary artery (LAD) and received normal saline (0.5 ml) as vehicle; the second MI model group were rats with LAD ligation and received normal saline (0. 5 ml) and the third one is MI+ghrelin group were rats that were exposed to surgery to induce MI but received ghrelin (100 /kg, orally, 2x/day). At the end of the experiment after 21 days post-MI, rats were sacrificed and processed for ultrastructural demonstration. Our experiment showed that ghrelin inhibited cardiomyocyte apoptosis. Concomitant administration of ghrelin with MI treated rats of this study appeared to show a considerable protection of the atrial tissues. This study revealed that the sarcoplasm was occupied by normal myofibrils with clear striations and others appeared with minor disruption. Normal distribution of atrionatriuretic factor (ANF) granules and well preserved mitochondrial integrity (preserved cristae, normal size and shape), nucleus chromatin arrangement and striated pattern of clear bands (Z and H) compared to the MI group. Intact intercalated disc with clear identification of fully formed fascia adherence and desmosomes with a reconstruction of gap junction (nexus) was also noticed. Atrial myocytes after myocardial infarction is often associated with subsequent heart failure, which could lead to a fatal outcome. In a rat model of experimental myocardial infarction, peripheral ghrelin administration attenuated myocyte dysfunction, well-preserved desmosome, adherent and gap junction of the intercalated disc and normally distributed ANF granules.
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Eid et al. (2018) studied Experimentally-induced Myocardial Infarction (n=60). Ghrelin vs. Normal saline was evaluated on Ultrastructural changes in atrial tissues (ANF granules, intercalated discs, apoptosis). Peripheral ghrelin administration in a rat model of experimental myocardial infarction attenuated myocyte dysfunction, preserved intercalated discs, and maintained normal distribution of ANF granules.
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