title: Partial left ventricular unloading reverses contractile dysfunction and helps recover gene expressions in failing rat hearts.
abstract: We investigated the effects of partial left ventricular unloading on failing rat hearts by using heterotopic heart-lung transplantation model. Heart failure (HF) was induced in Lewis rats by ligating the left anterior descending artery. After four weeks, the infarcted hearts and lungs were harvested and transplanted into the recipient rats by anastomosing donor's ascending aorta to recipient's abdominal aorta. Therefore, coronary venous blood entered the left ventricle (LV) and LV was partially unloaded (HF-PU group). Normal and infarcted heart rats (HF group) without transplantation served as control animals. After two weeks' unloading, the infarcted LV in HF-PU group significantly decreased its weight and myocardial diameter compared with HF group and they were close to normal levels. Developed tension of posterior papillary muscle was significantly increased in HF-PU group compared with HF group. The mRNA expressions of brain natriuretic peptide (BNP), sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA2a), beta(1) and beta(2)-adrenergic receptors (beta(1) and beta(2)-AR) in LV tissue were almost normalized in HF-PU group. Partial left ventricular unloading regressed myocardial hypertrophy, reversed contractile dysfunction and normalized the mRNA (BNP, SERCA2a, beta(1) and beta(2)-AR) expressions of failing rat hearts.
authors.affiliation: Department of Cardiovasular Surgery, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.
authors.forename: Jian
authors.initials: J
authors.lastname: Wang
authors.forename: Akira
authors.initials: A
authors.lastname: Marui
authors.forename: Tadashi
authors.initials: T
authors.lastname: Ikeda
authors.forename: Masashi
authors.initials: M
authors.lastname: Komeda
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D015870:Gene Expression; D006333:Heart Failure / Q000235:genetics / Q000503:physiopathology / Q000601:surgery*; D016027:Heart Transplantation / Q000379:methods*; D006352:Heart Ventricles / Q000378:metabolism / Q000503:physiopathology*; D009200:Myocardial Contraction / Q000502:physiology*; D020097:Natriuretic Peptide, Brain / Q000235:genetics / Q000378:metabolism; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D011917:Rats, Inbred Lew; D018342:Receptors, Adrenergic, beta-1 / Q000235:genetics / Q000378:metabolism; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics / Q000378:metabolism; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000235:genetics / Q000378:metabolism; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D012333:RNA, Messenger; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; D020097:Natriuretic Peptide, Brain; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases