Girard C, Fargnoli J M, Godin-Ribuot D, Dutheil V, Maitrasse B, Girardet P, Arvieux C C
Département d'Anesthésie Réanimation, Hôpital Cardiovasculaire et Pneumologique Louis Pradel, Lyon, France.
J Heart Lung Transplant. 1996 Jul;15(7):700-8.
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.
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.
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).
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.
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.
肺动脉高压合并右心室衰竭是心脏移植后立即出现的常见并发症,吸入一氧化氮可能有效。
在八只麻醉犬中评估肺动脉高压和一氧化氮对心肌功能以及肺和全身血流动力学参数的影响。通过向肺循环中连续注射微珠诱导肺动脉高压。
注射微珠导致明显的肺动脉高压(肺动脉压,升高190%;肺血管阻力,升高389%;肺血管阻力与体循环血管阻力之比,0.41)。
右心室流出道舒张末期长度随着右心室收缩力增加而显著增加(左心室压力随时间变化的峰值一阶导数,升高100%;流出道收缩期缩短,升高19%)。尽管有这种代偿机制,但增加的肺阻力导致每搏量减少(-31%)。观察到全身效应,如心率增加,尽管左心室舒张末期长度减少(左前降支区域的舒张末期长度,减少9%),但仍维持心输出量。右心肌和间隔血流也显著增加。
给予一氧化氮可恢复每搏量,同时降低肺动脉高压并改善肺血管阻力与体循环血管阻力之比。全身血压和冠状动脉灌注未受影响。这种对肺循环的选择性作用应被视为吸入一氧化氮治疗急性肺动脉高压中右心室功能障碍的主要优势。