Changes in cerebral blood flow trigger an increase in sympathetic nerve activity – implications following acute myocardial infarction

Heart function is controlled by the sympathetic nervous system. Following a heart attack (myocardial infarction: MI), cardiac sympathetic nerve activity (cSNA) becomes dangerously elevated, triggering irregular heartbeats (arrhythmias) that often prove fatal. In those who survive the initial MI, the sympathetic hyper-excitation is irreversible and facilitates permanent structural and functional damage of the heart. cSNA is ultimately driven by the brain and we have recently shown that the hypothalamic paraventricular nucleus (PVN) appears to facilitate this increase in SNA following MI. However, the trigger that activates these oxytocin neurons following MI remains to be determined. Neuronal activity is modulated by cerebral blood flow (CBF). CBF is impaired in chronic heart failure, which is thought to cause the sustained increase in cSNA. Hence, a sudden decrease in CBF following an MI may trigger PVN activation providing the drive for the increase in cSNA.

Research Question and Objectives
The overall aim of this study is to test the hypothesis that decreased CBF activates PVN neurons to increase cSNA following acute MI. Specifically, i) advanced Synchrotron Radiation microangiography (Hyogo, Japan) will be utilized to image the changes in cerebral blood flow associated with acute MI, ii) changes in CBF will be correlated with PVN activation (immunohistochemistry) and cSNA (electrophysiology).

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