Inhaled nitric oxide: effects on hemodynamics, myocardial contractility, and regional blood flow in dogs with mechanically induced pulmonary artery hypertension.
BACKGROUND
Pulmonary artery hypertension with right ventricular failure is a frequent complication that occurs immediately after heart transplantation in which the use of inhaled nitric oxide may be effective.


METHODS
The effects of pulmonary artery hypertension and nitric oxide on myocardial function and on pulmonary and systemic hemodynamic parameters were evaluated in eight anesthetized dogs. Pulmonary artery hypertension was induced by successive microbead injections into the pulmonary circulation.


RESULTS
Microbead injections resulted in overt pulmonary artery hypertension (pulmonary artery pressure, + 190%; pulmonary vascular resistance, + 389%; ratio of pulmonary vascular resistance to systemic vascular resistance, 0.41).


RESULTS
The end-diastolic length of the right ventricular outflow tract increased significantly along with an increase in right ventricular contractility (peak first derivative of left ventricular pressure as a function of time, + 100%; outflow tract systolic shortening, + 19%). Despite this compensatory mechanism, the increased pulmonary barrier resulted in a decrease in stroke volume (-31%). Systemic effects were observed, such as an increase in heart rate that maintained the cardiac output despite a decrease in left ventricular end-diastolic length (end-diastolic length in region of left anterior descending artery, - 9%). Right myocardial and septal blood flows were also significantly increased.


CONCLUSIONS
Nitric oxide administration restored the stroke volume with a decrease in pulmonary artery hypertension and an improvement of the pulmonary vascular resistance to systemic vascular resistance ratio. Systemic blood pressure and coronary perfusion remained unaffected. This selective effect on the pulmonary circulation should be considered a major advantage of nitric oxide inhalation in the treatment of right ventricular dysfunction in acute pulmonary hypertension.
Girard
C
C
Département d'Anesthésie Réanimation, Hôpital Cardiovasculaire et Pneumologique Louis Pradel, Lyon, France.
Fargnoli
J M
JM
Godin-Ribuot
D
D
Dutheil
V
V
Maitrasse
B
B
Girardet
P
P
Arvieux
C C
CC
D000208:Acute Disease; D000280:Administration, Inhalation; D000818:Animals; D004195:Disease Models, Animal; D004285:Dogs; D004353:Drug Evaluation, Preclinical; D006439:Hemodynamics / Q000187:drug effects*; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D009200:Myocardial Contraction / Q000187:drug effects*; D009569:Nitric Oxide / Q000008:administration & dosage* / Q000494:pharmacology; D011652:Pulmonary Circulation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000008:administration & dosage* / Q000494:pharmacology
D014665:Vasodilator Agents; D009569:Nitric Oxide