β2‐Adrenergic Receptor Expression on Hematopoietic Cells is Critical for Survival Following Myocardial Infarction

β‐adrenergic receptors (βAR) are critical regulators of cardiac function normally and during heart failure (HF). The importance of βAR on cardiomyocyte contractility and survival is well defined however, following myocardial infarction (MI), inflammatory responses occur, which are critical for healing and scar formation. Catecholamines acting through βAR, particularly the β2AR subtype, are known to modulate immune responses, however, the influence of β2AR in regulating the inflammatory response following MI is unknown. To investigate the contribution of β2AR on immune cells following MI, wild‐type (WT) mice were irradiated and then received β2AR knockout (KO) or WT control bone marrow (BM) transplants to create immune cell specific KO animals. Following BM reconstitution, mice were subjected to MI and cardiac function and survival were monitored. Cardiac function, as assessed by echocardiography, did not differ between WT and KO chimeric mice. However, mice lacking β2AR in their BM resulted in 100% mortality from cardiac rupture within two weeks of receiving MI in contrast to their WT counterparts that had ~20% death. Masson trichrome staining demonstrated infarct expansion in KO chimeric mice was more rapid than their WT counterparts. While there was no change in total cell infiltration into the heart following MI, a retention of granulocytes occurred in the spleen of KO chimeric mice resulting in reductions in infiltrating leukocyte populations. Alterations CCR2 on KO BM resulted in decreased cellular migration which could be rescued using a β2AR lentivirus to re‐express the β2AR. These results demonstrate the critical role of β2AR in mounting an immune response and promoting healing following MI.