Acute myocardial infarction (MI) triggers an adverse increase in cardiac sympathetic nerve activity (SNA). While β-adrenergic receptor (β-AR)-blockers are routinely used for the management of MI, they may also counter β-AR-mediated vasodilation of coronary vessels. We have reported that ghrelin prevents sympathetic activation following MI. Whether ghrelin modulates coronary vascular tone following MI, either through the modulation of SNA, or directly as a vasoactive mediator, has never been addressed.We utilized synchrotron microangiography to image coronary perfusion and vessel internal diameter (ID) in anesthetized Sprague Dawley rats before, and then again 30 mins after induction of an MI (left coronary artery ligation). Rats were injected with either saline or ghrelin (150 µg/kg, s.c.) immediately following the MI or sham surgery. Coronary angiograms were also recorded following β-AR blockade (propranolol, 2 mg/kg, i.v.). Finally, wire myography was used to assess the effect of ghrelin on vascular tone in isolated human internal mammary arteries (IMA). Acute MI enhanced coronary perfusion to 'non-ischemic' regions through dilation of small arterioles (ID 50-250 µm) and microvessel recruitment; irrespective of ghrelin treatment. In ghrelin-treated rats, β-AR blockade did not alter the ischemia-induced vasodilation, yet in saline-treated rats, β-AR blockade abolished the vasodilation of small arterioles. Finally, ghrelin caused a dose-dependent vasodilation of IMA rings (pre-constricted with phenylephrine). In summary, this study highlights ghrelin as a promising adjunct therapy, that can be utilized in combination with routine β-AR blockade treatment, for preserving coronary blood flow and cardiac performance in patients that suffer an acute myocardial infarction.
This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 02 February 2018.
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