Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0613820180280020240
Journal of Life Science
2018 Volume.28 No. 2 p.240 ~ p.246
Renal Sympathetic Denervation Induces Acute Myocardial Inflammation through Activation of Caspase-1 and Interleukin-1¥â
Lee Dong-Won

Kim Il-Young
Kwak Ihm-Soo
Abstract
Efferent and afferent sympathetic nerves are closely related to the development of hypertension and heart failure. Catheter-based renal sympathetic denervation (RDN) is implemented as a strategy to treat resistant hypertension. We investigated whether RDN procedure causes inflammatory damage on myocardium in the early phase of sympathetic denervation. Twenty-five female swine were divided into 3 groups: normal control (Normal, n=5), sham-operated control (Sham, n=5), and RDN groups (RDN, n=15). The RDN group was further subdivided into 3 subgroups according to the time of sacrifice: immediately (RDN-0, n=5), 1 week (RDN-1, n=5), and 2 weeks (RDN-2, n=5) after RDN. There were no significant changes in the clinical parameters between the normal control and sham-operated group using contrast-media. In the myocardium, inflammatory cytokines, IL-1¥â and TNF-¥á increased at the first week, and then decreased at the second week after RDN. Anti-inflammatory cytokine, IL-10 increased immediately, and then decreased at the second week after RDN. Caspase-1 activity and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) expression increased immediately after RDN until the second week. However, nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing protein 3 (NLRP3) expression did not show any significant differences among the groups. The RDN can cause acute myocardial inflammation through activation of caspase-1 and IL-1¥â. We should pay attention to protecting against early inflammatory myocardial damage after RDN.
KEYWORD
Cytokines, heart failure, inflammasomes, myocardium, sympathectomy
FullTexts / Linksout information
Listed journal information
ÇмúÁøÈïÀç´Ü(KCI)