Schreiber Michael D, Dixit Rajeev, Rudinsky Brian, Hipps Robert, Morgan Sherwin E, Keith RRT Alfred, Meadow William
Department of Pediatrics, University of Chicago, IL 60637, USA.
Crit Care Med. 2002 Nov;30(11):2560-5. doi: 10.1097/00003246-200211000-00026.
To test the hypothesis that nebulized nitroprusside and inhaled nitric oxide would not differ in producing selective pulmonary vasodilation during hypoxia-induced pulmonary hypertension in piglets.
University laboratory.
Five piglets.
Piglets (n = 5) were anesthetized and instrumented to monitor systemic arterial pressure, pulmonary artery pressure, and cardiac output continuously. Hypoxia was induced (DeltaFio2 from 0.5 to 0.08), and either nebulized nitroprusside (5 mg/mL at 4 L/min flow; total dose 25 mg) or inhaled nitric oxide (20 ppm) was introduced into the ventilator circuit for 15 mins. Normoxia was then restored, and a repeat cycle of hypoxia followed by the alternate vasodilator treatment was initiated.
Hypoxia significantly reduced Pao2 (from 206 to 30 torr) and elevated pulmonary artery pressure (from 18 to 33 torr) while not significantly affecting systemic arterial pressure or cardiac output. During hypoxia, inhaled nitric oxide reduced pulmonary artery pressure from 33 to 21 torr (p <.01), whereas systemic arterial pressure and cardiac output were unchanged. During hypoxia, nebulized nitroprusside also reduced pulmonary artery pressure from 33 to 23 mm Hg (p <.01; p = nonsignificant vs. inhaled nitric oxide), whereas systemic arterial pressure and cardiac output again remained constant. The time course of the reduction in pulmonary artery pressure during inhaled nitric oxide was roughly ten-fold more rapid (<5 secs) than during nebulized nitroprusside ( approximately 1 min). Neither inhaled nitric oxide nor nebulized nitroprusside altered pH, Pao2, or Paco2.
Both inhaled nitric oxide and nebulized nitroprusside produced prompt, significant, selective reduction of pulmonary artery pressure and pulmonary vascular resistance in piglets with hypoxia-induced pulmonary hypertension, without apparent effects on systemic hemodynamics or pulmonary gas exchange. The equivalence of the two effects in this animal model suggests that cautious extrapolation of the use of nebulized nitroprusside as a convenient bridge to inhaled nitric oxide in selected clinical contexts for human infants may be warranted.
验证在仔猪缺氧诱导的肺动脉高压期间，雾化硝普钠和吸入一氧化氮在产生选择性肺血管舒张方面无差异这一假设。
大学实验室。
5头仔猪。
将仔猪（n = 5）麻醉并安装仪器以持续监测体动脉压、肺动脉压和心输出量。诱导缺氧（吸入氧分数从0.5降至0.08），然后将雾化硝普钠（5 mg/mL，流速4 L/min；总剂量25 mg）或吸入一氧化氮（20 ppm）引入通气回路15分钟。随后恢复常氧，接着启动重复的缺氧周期，之后交替进行血管舒张剂治疗。
缺氧显著降低了动脉血氧分压（从206降至30 torr）并升高了肺动脉压（从18升至33 torr），而对体动脉压或心输出量无显著影响。在缺氧期间，吸入一氧化氮使肺动脉压从33降至21 torr（p <.01），而体动脉压和心输出量未改变。在缺氧期间，雾化硝普钠也使肺动脉压从33降至23 mmHg（p <.01；与吸入一氧化氮相比p无显著差异），而体动脉压和心输出量再次保持恒定。吸入一氧化氮期间肺动脉压降低的时间进程比雾化硝普钠期间（约1分钟）快约10倍（<5秒）。吸入一氧化氮和雾化硝普钠均未改变pH、动脉血氧分压或动脉血二氧化碳分压。
吸入一氧化氮和雾化硝普钠均可使缺氧诱导的肺动脉高压仔猪的肺动脉压和肺血管阻力迅速、显著且选择性降低，对体循环血流动力学或肺气体交换无明显影响。在该动物模型中两种效应的等效性表明或许有必要谨慎推断在特定临床情况下将雾化硝普钠作为人类婴儿吸入一氧化氮的便捷过渡手段的应用。
