Testosterone therapy improves cardiac function of male rats with right heart failure.
- Author:
Zong-Bin LI
1
;
Jing WANG
;
Ju-Xiang WANG
;
Xun-Min CHEN
;
Shi-Sen JIANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Heart Failure; drug therapy; metabolism; Male; Rats; Rats, Sprague-Dawley; Testosterone; blood; therapeutic use; Tumor Necrosis Factor-alpha; blood
- From: National Journal of Andrology 2009;15(11):994-1000
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEClinical studies have shown decreased levels of sexual hormones, particularly testosterone deficiency, in men with chronic heart failure (CHF). The authors aimed to investigate the effect of testosterone on cardiac function and the possible mechanism of androgen protecting the heart in male rats.
METHODSForty-three male SD rats were randomly divided into 3 groups: right heart failure (RHF, n = 15), physiologic testosterone treatment (TT, n = 15) and control (n = 13). The RHF group was given intraperitoneal injection of monocrotaline at 60 mg/kg to make RHF models; the TT group was injected with testosterone at 5 mg/kg 3 days after monocrotaline administration; and the control group received equal volume of saline. The CD34+ cells in the peripheral blood of each rat were counted by flow cytometry. The levels of serum testosterone and tumor necrosis factor alpha (TNF-alpha) were measured by chemiluminescence immunoassay and enzyme linked immunosorbent assay, respectively. The hearts, lungs and livers of all the surviving rats were excised at 6 weeks for pathological and immunohistochemical examinations.
RESULTSThe level of serum testosterone was gradually decreased, while that of TNF-alpha obviously increased in the RHF group. After testosterone treatment, the TT group showed a remarkable improvement of cardiac performance and a significant decrease in the level of serum TNF-alpha as compared with the RHF group. Statistically significant differences were observed neither in the CD34+ cell count in the peripheral blood nor in the CD34+ expression of the myocardial cells between the TT and RHF groups.
CONCLUSIONPhysiological supplementation of testosterone can improve the cardiac function of RHF male rats, probably through its inhibition of TNF-alpha rather than by autologous mobilization of bone marrow stem cells.