This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Jian Wang Tadashi Ikeda Masashi Komeda Permission Requests Google Scholar Articles by Wang, J. Articles by Komeda, M. PubMed PubMed Citation Articles by Wang, J. Articles by Komeda, M. Related Collections Cardiac - physiology Mechanical Circulatory Assistance Myocardial infarction Transplantation - heart

Partial left ventricular unloading reverses contractile dysfunction and helps recover gene expressions in failing rat hearts

Department of Cardiovasular Surgery, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan

*Corresponding author. Tel.: +81-75-751-3784; fax: +81-75-751-4960.

E-mail address: komelab{at}kuhp.kyoto-u.ac.jp (M. Komeda).

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 Ca²⁺-ATPase (SERCA2a), β₁ and β₂-adrenergic receptors (β₁ and β₂-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, β₁ and β₂-AR) expressions of failing rat hearts.

Key Words: Heart failure; Heart-assist device; Myocardial contraction; Remodeling; Genes