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2018 ; 114
(2
): 291-299
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Local sympathetic denervation attenuates myocardial inflammation and improves
cardiac function after myocardial infarction in mice
#MMPMID29186414
Ziegler KA
; Ahles A
; Wille T
; Kerler J
; Ramanujam D
; Engelhardt S
Cardiovasc Res
2018[Feb]; 114
(2
): 291-299
PMID29186414
show ga
AIMS: Cardiac inflammation has been suggested to be regulated by the sympathetic
nervous system (SNS). However, due to the lack of methodology to surgically
eliminate the myocardial SNS in mice, neuronal control of cardiac inflammation
remains ill-defined. Here, we report a procedure for local cardiac sympathetic
denervation in mice and tested its effect in a mouse model of heart failure
post-myocardial infarction. METHODS AND RESULTS: Upon preparation of the carotid
bifurcation, the right and the left superior cervical ganglia were localized and
their pre- and postganglionic branches dissected before removal of the ganglion.
Ganglionectomy led to an almost entire loss of myocardial sympathetic innervation
in the left ventricular anterior wall. When applied at the time of myocardial
infarction (MI), cardiac sympathetic denervation did not affect acute myocardial
damage and infarct size. In contrast, cardiac sympathetic denervation
significantly attenuated chronic consequences of MI, including myocardial
inflammation, myocyte hypertrophy, and overall cardiac dysfunction. CONCLUSION:
These data suggest a critical role for local sympathetic control of cardiac
inflammation. Our model of myocardial sympathetic denervation in mice should
prove useful to further dissect the molecular mechanisms underlying cardiac
neural control.