title: Degree of external force to the left ventricle determines hemodynamic response to nitroprusside in failing hearts: comparison with the response to dobutamine.
abstract: Vasodilators frequently, although not always, increase cardiac output (CO) in patients with congestive heart failure (CHF) despite a decrease in left ventricular (LV) diastolic pressure. In patients with CHF, vasodilator-induced decrease in LV diastolic pressure without decrease in "preload" plays an important role in the vasodilator-induced increase in CO failure that may be caused by a vasodilator-induced reduction in external force to the LV. To clarify the hypothesis that a hemodynamic response to vasodilators depends on the degree of external force to the LV in failing hearts before drug administration and to examine whether the degree of the external force also affects a hemodynamic response to positive inotropic agents, we produced in 17 dogs two different conditions of LV dysfunction with high LV end-diastolic pressure (EDP: > or = 15 mm Hg), i.e., 1 with high right ventricular (RV) EDP (condition 1) and the other with lower RVEDP than condition 1 (condition 2), and compared hemodynamic effects of nitroprusside or dobutamine between these two conditions. Condition 1 was produced by the injection of a small dose of microspheres into the left coronary artery and intravenous infusion of dextran. Condition 2 was produced only by the injection of a large dose of microspheres. The nitroprusside-induced decrease in LVEDP was associated with a greater decrease in RVEDP and lesser decreases in mean left atrial pressure and LV end-diastolic diameter in condition 1 than in condition 2. CO increased in condition 1; however, CO then decreased in condition 2. The nitroprusside-induced changes in CO inversely correlated with those in RVEDP (r = 0.65, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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: R
authors.initials: R
authors.lastname: Nagano
authors.forename: Y
authors.initials: Y
authors.lastname: Doi
authors.forename: J
authors.initials: J
authors.lastname: Naito
authors.forename: T
authors.initials: T
authors.lastname: Mano
authors.forename: H
authors.initials: H
authors.lastname: Kondo
authors.forename: M
authors.initials: M
authors.lastname: Hori
authors.forename: T
authors.initials: T
authors.lastname: Kamada
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D004195:Disease Models, Animal; D004280:Dobutamine / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D004285:Dogs; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D008863:Microspheres; D009599:Nitroprusside / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D011312:Pressure; D011897:Random Allocation; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D002316:Cardiotonic Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D004280:Dobutamine