Beghetti M, Habre W, Friedli B, Berner M
Department of Paediatrics, Hôpital Cantonal Universitaire, Geneva, Switzerland.
Br Heart J. 1995 Jan;73(1):65-8. doi: 10.1136/hrt.73.1.65.
To assess the effect of inhaled nitric oxide (NO) on severe postoperative pulmonary hypertension in children after surgical repair of a congenital heart defect.
A pilot study of NO administration to 7 consecutive children who required adrenergic support and in whom postoperative mean pulmonary artery pressure was more than two thirds of mean systemic pressure and persisted despite alkalotic hyperventilation.
Routine care after cardiac surgery for congenital heart disease in a multidisciplinary paediatric intensive care unit.
Continuous inhalation of NO, initially at 15 ppm. Therefore, daily attempts at complete weaning or at reducing NO to the lowest effective dose.
In 6 of the 7 children NO inhalation selectively decreased mean (SD) pulmonary artery pressure from 51 (12) to 31 (9) mm Hg (P < 0.05) while mean systemic arterial pressure was unchanged (68 (10) v 71 (7) mm Hg) (NS) and the arteriovenous difference in oxygen content decreased from 6.7 (0.9) to 4.8 (0.8) vol% (P < 0.05). Concomitantly PaO2 increased from 158 (98) to 231 (79) mm Hg) (P < 0.05). The seventh child showed no response to NO up to 80 ppm, could not be weaned from cardiopulmonary bypass, and died in the operating room. In responders, attempts at early weaning from NO inhalation always failed and NO at concentrations of less than 10 ppm was continuously administered for a median of 9.5 days (range 4 to 16 days) until complete weaning was possible from a mean dose of 3.9 (2.9) ppm. Methaemoglobinaemia remained below 2% and nitrogen dioxide concentrations usually ranged from 0.1 to 0.2 ppm. One child later died and five were discharged. A few months after surgery Doppler echocardiography (and catheterisation in one) showed evidence of regression of pulmonary hypertension in all 5.
Inhalation of NO reduced pulmonary artery pressure in children with severe pulmonary hypertension after cardiac surgery and this effect was maintained over several days at concentrations carrying little risk of toxicity.
评估吸入一氧化氮（NO）对先天性心脏病手术修复术后儿童严重肺动脉高压的影响。
一项对7例连续患儿进行的NO给药初步研究，这些患儿需要肾上腺素能支持，且术后平均肺动脉压超过平均体循环压力的三分之二，尽管进行了碱中毒过度通气仍持续存在。
在多学科儿科重症监护病房对先天性心脏病进行心脏手术后的常规护理。
持续吸入NO，初始浓度为15 ppm。因此，每日尝试完全撤机或降低NO至最低有效剂量。
7例患儿中的6例吸入NO后，平均（标准差）肺动脉压从51（12）降至31（9）mmHg（P<0.05），而平均体循环动脉压未改变（68（10）对71（7）mmHg）（无统计学差异），动静脉氧含量差从6.7（0.9）降至4.8（0.8）vol%（P<0.05）。同时，动脉血氧分压从158（98）升至231（79）mmHg（P<0.05）。第7例患儿对高达80 ppm的NO无反应，无法脱离体外循环，死于手术室。在有反应的患儿中，早期尝试停止吸入NO均失败，持续给予浓度低于10 ppm的NO，中位时间为9.5天（范围4至16天），直至能够从平均剂量3.9（2.9）ppm完全撤机。高铁血红蛋白血症保持在2%以下，二氧化氮浓度通常在0.1至0.2 ppm之间。1例患儿后来死亡，5例出院。术后几个月，多普勒超声心动图（1例进行了心导管检查）显示所有5例患儿的肺动脉高压均有消退迹象。
吸入NO可降低心脏手术后严重肺动脉高压患儿的肺动脉压，且在毒性风险极小的浓度下，这种作用可维持数天。
