Why the study?
The mechanism of the no reflow phenomenon after treatment of acute myocardial infarction is unknown, despite its association with worse outcomes.
Does GPR39 inhibition or knockout reduce no-reflow zones and infarct size in animal models of acute myocardial infarction?
Does GPR39 inhibition or knockout reduce no-reflow zones and infarct size in animal models of acute myocardial infarction?
Answers are grounded in this paper and cite their sources.
Inhibition of GPR39-mediated pericyte contraction represents a potential therapeutic strategy to prevent the 'no reflow' phenomenon and reduce infarct size after acute myocardial infarction.
The mechanism of "no reflow" phenomenon, where the coronary artery is patent after treatment of acute myocardial infarction but tissue perfusion is not restored, is unknown. This condition is associated with worse outcome. Here, we show that GPR39-mediated pericyte contraction during reduced coronary perfusion pressure causes capillary constriction resulting in no reflow. Smaller no-reflow zones in GPR39-knockout animals and those treated with a GPR39 inhibitor are associated with smaller infarct size. These results could have important therapeutic implications.
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Methner et al. (2021) studied this question.
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