title: Inhaled nitric oxide modifies left ventricular diastolic stress in the presence of vasoactive agents in heart failure.
abstract: Nitric oxide (NO) inhalation therapy has been widely used in several diseases with pulmonary hypertension. However, application of NO inhalation therapy remains controversial in heart failure. Cardiovascular effects of inhaled NO (iNO) were evaluated in dogs before and after induction of heart failure with and without infusion of vasoactive agents. iNO did not affect the baseline left ventricular (LV) function or the response to isoproterenol in control conditions or heart failure induced by procainamide. Pulmonary vascular resistance was significantly decreased by iNO in heart failure with infusion of vasoactive agents. Unexpectedly, LV end-diastolic pressure was significantly elevated by iNO in heart failure in the presence of infusion of vasoactive agents independent of their types; either the vasodilating agents of acetylcholine and nitroglycerin or the vasoconstricting agents of norepinephrine and angiotensin-II. The end-diastolic LV dimension and wall stress were also significantly increased by iNO, however, those at end systole were not affected. These results suggested that NO inhalation therapy reduced pulmonary vascular resistance, whereas in the presence of additional stress of vasoactive agents, it increased LV preload and end-diastolic wall stress in heart failure.
authors.affiliation: First Department of Internal Medicine, Asahikawa Medical College, 2-1-1-1 Midorigaoka higashi, Asahikawa, Hokkaido 078-8510, Japan. haselove@asahikawa-med.ac.jp
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Natori
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Hasebe
authors.forename: Yin-Tie
authors.initials: YT
authors.lastname: Jin
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Matsusaka
authors.forename: Akira
authors.initials: A
authors.lastname: Ido
authors.forename: Hironobu
authors.initials: H
authors.lastname: Matsuhashi
authors.forename: Tadashi
authors.initials: T
authors.lastname: Ihara
authors.forename: Kenjiro
authors.initials: K
authors.lastname: Kikuchi
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage / Q000494:pharmacology; D000280:Administration, Inhalation; D000804:Angiotensin II / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D003971:Diastole / Q000187:drug effects*; D004195:Disease Models, Animal; D004285:Dogs; D004353:Drug Evaluation, Preclinical; D005260:Female; D006333:Heart Failure / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D007262:Infusions, Intravenous; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009569:Nitric Oxide / Q000008:administration & dosage* / Q000494:pharmacology; D005996:Nitroglycerin / Q000008:administration & dosage / Q000494:pharmacology; D009638:Norepinephrine / Q000008:administration & dosage / Q000494:pharmacology; D011342:Procainamide / Q000009:adverse effects; D011652:Pulmonary Circulation / Q000187:drug effects; D011897:Random Allocation; D013318:Stroke Volume / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000494:pharmacology; D014665:Vasodilator Agents / Q000008:administration & dosage* / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000804:Angiotensin II; D009569:Nitric Oxide; D005996:Nitroglycerin; D011342:Procainamide; D007545:Isoproterenol; D000109:Acetylcholine; D009638:Norepinephrine