[Effects of humoral factors on left ventricular remodeling under chronic heart failure].
Chronic heart failure is a slowly progressive disease. Hemodynamic deterioration activates various neuro-humoral factors and increases stresses, such as catecholamine, angiotensin II (AII), cytokines, endothelin, wall stress, ischemia, tachycardia, and oxidative stress. These factors affect the myocardium to cause phenotype switching, leading to ventricular remodeling. We investigated the effects of pharmacological blocking for neuro-humoral factors in rats with dilated cardiomyopathy. Experimental autoimmune myocarditis (EAM) was elicited in Lewis rats by immunization with cardiac myosin. After acute inflammation healed, rats were treated with angiotensin converting enzyme inhibitors (ACEI), type 1 AII receptor blockers, and amiodarone. These agents had favorable effects on hemodynamics and myocardial contractility, prevented fibrosis, suppressed the expression of ANP, and reversed phenotypic change of cardiac myosin. AII receptor blockers were less effective than ACEI. In order to prevent ventricular remodeling in chronic heart failure, wide and complete blocking of neuro-humoral factors is important.
Kodama
Makoto
M
Division of Cardiology, Niigata University Graduate School of Medical & Dental Sciences, Japan. kodamama@med.niigata-u.ac.jp
Tachikawa
Hitoshi
H
Kashimura
Takeshi
T
Hayashi
Manabu
M
Yoshida
Tsuyoshi
T
Hanawa
Haruo
H
Aizawa
Yoshifusa
Y
Nakazawa
Mikio
M
Watanabe
Kenichi
K
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002908:Chronic Disease; D016207:Cytokines / Q000502:physiology; D006333:Heart Failure / Q000503:physiopathology*; D006439:Hemodynamics; D051381:Rats; D020257:Ventricular Remodeling / Q000502:physiology
D000806:Angiotensin-Converting Enzyme Inhibitors; D016207:Cytokines