title: Role of basal release of nitric oxide in the presence of acute left ventricular dysfunction: comparative study with normal condition.
abstract: The basal release of nitric oxide (NO) plays an important role in the regulation of vascular circulation in the presence of acute left ventricular dysfunction. It is not clear, however, whether the role is as important in the presence of acute left ventricular dysfunction as it is in the normal condition. In addition, the effects of flow rate on the role of basal NO have not been clarified in the presence of acute left ventricular dysfunction. This in vivo study was attempted to compare the contribution of the basal release of NO to the regulation of vascular circulation and the effects of a mechanically reduced basal flow rate on the contribution of basally released NO between the normal condition and acute left ventricular dysfunction. In eight anesthetized dogs, the responses of femoral artery blood flow to NG-monomethyl-L-arginine (L-NMMA, 10(-5)M) were observed with and without a reduction in basal flow. The same observation was performed after the production of acute left ventricular dysfunction by coronary microembolization. Without the reduction in basal flow, the L-NMMA-induced decrease in femoral artery flow was significantly larger in acute left ventricular dysfunction than in the normal condition (-40 +/- 12% vs-17 +/- 6%, P < .01). Under the reduction in basal flow, there was no significant change in flow during the infusion of L-NMMA in the normal condition and only a small decrease in acute left ventricular dysfunction. There was no significant difference in the L-NMMA-induced changes in flow between these conditions. The contribution of basally released NO to the regulation of vascular circulation is larger in the presence of acute left ventricular dysfunction than in the normal condition; however, the role of basal NO is reduced with a decrease in basal flow rate.
authors.affiliation: First Department of Medicine, Osaka University School of Medicine, Suita, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Yamamoto
authors.forename: T
authors.initials: T
authors.lastname: Masuyama
authors.forename: T
authors.initials: T
authors.lastname: Mano
authors.forename: J
authors.initials: J
authors.lastname: Naito
authors.forename: H
authors.initials: H
authors.lastname: Kondo
authors.forename: R
authors.initials: R
authors.lastname: Nagano
authors.forename: M
authors.initials: M
authors.lastname: Hori
authors.forename: T
authors.initials: T
authors.lastname: Kamada
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000208:Acute Disease; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D004285:Dogs; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005263:Femoral Artery; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D011897:Random Allocation; D018487:Ventricular Dysfunction, Left / Q000378:metabolism*; D016277:Ventricular Function, Left / Q000502:physiology*; D019323:omega-N-Methylarginine
chemical_list: D004791:Enzyme Inhibitors; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D000109:Acetylcholine