2002 Fiscal Year Final Research Report Summary
Alterations of the functions of imidazoline-1 and alpha 2 adrenergic receptors in the medulla oblongata in the development of heart failure
| Project/Area Number |
12670702
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Nippon Medical School |
|---|
Principal Investigator |
SATO Naoki Nippon Medical School, Medicine, Lecturer, 医学部, 講師 (70291721)
|
|---|
| Project Period (FY) |
2000 – 2002
|
| Keywords | Heart Failure / Imidazoline receptor / alpha2 adrenergic receptor |
|---|
| Research Abstract |
Background/Goal : Sympathetic activation is a hallmark of heart failure (HF). Clinical investigation have demonstrated usefulness of beta-blocker treatment for HF. However, it has not been well established whether nor not central symapthoinhibition could be favorable for the progression of HF, although it is known that activation of imidazoline receptors in central nervous system suppresses sympathetic outflow and decreases plasma norepinephrine levels. Therefore, our goal was to examine the effects of chronic administration of an imidazoline receptor agonist, rilmenidine (RIL), on HF in conscious beagles.
Methods : Twelve beagles were chronically instrumented for intra-atrial infusions of saline or RIL (0.5mg/kg/day over 5 weeks) and rapid pacing at 250 bpm. Echocardiography was performed before and after HF for measurements of left ventricular ejection fraction (LVEF), % fractional shortening (%FS), and LF end-diastolic dimension (EDD).
Results : Heart rate, %FS, LVEF, and EDD between control (C, n=6) and RIL(n=6) groups were not different before HF (C:126±31,38.1±9.0,68.1±11.0,35.6±3.5, RIL:121±17bpm,39.7±6.6%,70.8±7.9%,33.4±4.1mm, respectively). LV functions (%FS, LVEF, and EDD) in RIL group was significantly (p<0.05) better than C (15.3±6.9 vs 7.7±2.4%,32.5±12.5 vs 17.2±5.2%,4.5±5.0 vs 48.0±2.0 mm, respectively).
Conclusion : Central sympathoinhibition tolerated the development of HF, suggesting chronic suppression of symapthetiv outflow might be useful for the treatment of HF.
|
Research Products
(2 results)
