This Article Full Text (PDF) References 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 Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Yamamoto, K. Articles by Kamada, T. Search for Related Content PubMed PubMed Citation Articles by Yamamoto, K. Articles by Kamada, T. Social Bookmarking                         What's this?

Basal Release of Endothelium-Derived Nitric Oxide Plays an Important Role in the Prevention of Afterload Mismatch in Acute Left Ventricular Dysfunction

The First Department of Medicine, Osaka University School of Medicine, Suita, Japan

Tohru Masuyama

The First Department of Medicine, Osaka University School of Medicine, Suita, Japan

Toshiaki Mano

The First Department of Medicine, Osaka University School of Medicine, Suita, Japan

Johji Naito

The First Department of Medicine, Osaka University School of Medicine, Suita, Japan

Hiroya Kondo

The First Department of Medicine, Osaka University School of Medicine, Suita, Japan

Reiko Nagano

The First Department of Medicine, Osaka University School of Medicine, Suita, Japan

Jun Tanouchi

The First Department of Medicine, Osaka University School of Medicine, Suita, Japan

Masatsugu Hori

The First Department of Medicine, Osaka University School of Medicine, Suita, Japan

Takenobu Kamada

The First Department of Medicine, Osaka University School of Medicine, Suita, Japan

The basal release of endothelium-derived nitric oxide (EDNO) is considered to play an important role in regulating the vascular tone in normal subjects; however, its role in the presence of acute heart failure is unknown. This study was designed to clarify the role of a basal release of EDNO in the presence of acute heart failure. Acute ischemic left ventric ular (LV) dysfunction was produced in 22 dogs by coronary microembolization. After the embolization, only saline solution was intravenously infused for sixty minutes in 10 dogs. In another 12 dogs, NG-monomethyl-L-arginine (L-NMMA), which is known to inhibit the formation of EDNO in the vascular endothelium, was intravenously infused at a rate of 20 µg/kg/minute for sixty minutes. Infusion of saline solution did not produce any changes in hemodynamic variables. Infusion of L-NMMA caused increases in mean aortic pressure, systemic vascular resistance, and LV end-diastolic pressure without changes in the LV peak + and - dP/dt (time constant) of LV pressure fall, and these changes were associated with a giant "v" wave in the tracing of left atrial pressure and a decrease in cardiac output. The basal release of EDNO may play an important role in the prevention of afterload elevation, subsequent cardiac output reduction, and afterload mismatch in the presence of acute heart failure.

Angiology, Vol. 46, No. 9, 767-777 (1995)
DOI: 10.1177/000331979504600902


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?