Study summary · research use only
Hexarelin treatment in male ghrelin knockout mice after myocardial infarction
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study in male ghrelin-knockout mice examined whether hexarelin treatment could compensate for ghrelin deficiency after myocardial infarction, comparing hexarelin (400 nmol/kg/d, sc) and equimolar ghrelin treatment against vehicle for 2 weeks following left coronary artery ligation. Two-week mortality was lower with hexarelin (6.7%) and ghrelin (14.3%) than vehicle (50%) (P < .05). At 2 weeks, cardiac output, ejection fraction, and dP/dt min were greater with ghrelin and hexarelin than vehicle (P < .05), hexarelin showing larger changes than ghrelin in ejection fraction, dP/dt max, and dP/dt min. Sympathetic activity, by telemetry and heart rate variability, was suppressed in both treated groups versus vehicle. Hexarelin resulted in better heart function than ghrelin at 2 weeks, though the two hormones had similar effects on heart rate variability and mortality.
Abstract
Both ghrelin and the synthetic analog hexarelin are reported to possess cardioprotective actions that are mainly exerted through different receptors. However, their effects on acute myocardial infarction have not been compared in vivo. This study aimed to clarify whether hexarelin treatment can compensate for ghrelin deficiency in ghrelin-knockout mice and to compare the effects of hexarelin (400 nmol/kg/d, sc) and equimolar ghrelin treatment after myocardial infarction. Myocardial infarction was produced by left coronary artery ligation in male ghrelin-knockout mice, which then received ghrelin, hexarelin, or vehicle treatment for 2 weeks. The mortality within 2 weeks was significantly lower in the hexarelin group (6.7%) and ghrelin group (14.3%) than in the vehicle group (50%) (P < .05). A comparison of cardiac function 2 weeks after infarction showed that in the ghrelin and hexarelin treatment groups, cardiac output was greater, whereas systolic function, represented by ejection fraction, and diastolic function, represented by dP/dt min (peak rate of pressure decline), were significantly superior compared with the vehicle group (P < .05). Hexarelin treatment was more effective than ghrelin treatment, as indicated by the ejection fraction, dP/dt max (peak rate of pressure rise), and dP/dt min. Telemetry recording and heart rate variability analysis demonstrated that sympathetic nervous activity was clearly suppressed in the hexarelin and ghrelin groups relative to the vehicle group. Our data demonstrated that hexarelin treatment can result in better heart function than ghrelin treatment 2 weeks after myocardial infarction in ghrelin-knockout mice, although both hormones have similar effects on heart rate variability and mortality.
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