Effects of estrogen on venous function in rats with chronic heart failure

Citation
Aa. Nekooeian et Ccy. Pang, Effects of estrogen on venous function in rats with chronic heart failure, AM J P-HEAR, 278(6), 2000, pp. H1941-H1947
Citations number
50
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
278
Issue
6
Year of publication
2000
Pages
H1941 - H1947
Database
ISI
SICI code
0363-6135(200006)278:6<H1941:EOEOVF>2.0.ZU;2-A
Abstract
The effect of 17 beta-estradiol on venous function was investigated in ovar iectomized rats with heart failure. Rats (50-60 days old) were ovariectomiz ed and implanted with 60-day-release pellets that contain 17 beta-estradiol (1.5 mg) or vehicle. The left coronary artery was ligated 7 days later. An other group of ovariectomized rats was given vehicle pellets and then a sha m operation was performed. The rats were studied while under pentobarbital anesthesia at 7 wk after ligation. Ligated rats, relative to sham groups, h ad lower mean arterial pressure (MAP, -34 mmHg) and cardiac output (CO, -38 %); higher arterial resistance (R-A, +12%) and venous resistance (R-V, +116 %); mean circulatory filling pressure (MCFP, +40%) and left ventricular end -diastolic pressure (LVEDP, +11 mmHg); and similar cardiovascular responses to norepinephrine (NE). Treatment of ligated rats with 17 beta-estradiol i ncreased CO (+16%); reduced R-A (-16%), R-V (-35%), MCFP (-23%), and LVEDP (-3 mmHg); and augmented MAP, R-V, and MCFP responses to NE. Therefore, 17 beta-estradiol reduced MCFP, and this reduced preload (LVEDP). 17 beta-Estr adiol decreased R-V, which, along with decreased R-A (afterload), led to an increase in CO. 17 beta-Estradiol likely augmented vasoconstriction to NE through an improvement on the cardiovascular status.