Rayhrer C S, Edmisten T D, Cephas G A, Tribble C G, Kron I L, Young J S
Department of Surgery, University of Virginia Health Sciences Center, Charlottesville 22906-0005, USA.
Ann Thorac Surg. 1998 Apr;65(4):935-8. doi: 10.1016/s0003-4975(98)00119-2.
The effect of inhaled nitric oxide (NO) treatment on pulmonary function in the setting of adult respiratory distress syndrome is controversial. We examined the effect of inhaled NO on pulmonary function in an isolated rabbit lung model of oleic acid (OA)-induced acute lung injury. We hypothesized that NO would decrease pulmonary artery pressure and improve oxygenation.
Rabbit heart-lung blocks were isolated, flushed in vivo, harvested, and immediately perfused with whole blood and ventilated with 50% oxygen (O2). Pulmonary artery pressure was determined every 15 seconds for 60 minutes of perfusion. Oxygenation was determined by blood gas analysis of pulmonary venous effluent at 0, 20, 40, and 60 minutes after initiation of OA infusion. Rabbits were randomized into four study groups: saline control; OA control, which received a 20-minute infusion of 50% OA/ethanol solution; NO treatment (20 ppm NO inhaled before OA infusion); and NO control, which underwent NO (20 ppm) pretreatment, followed by saline infusion. Pulmonary artery pressure, oxygenation (arteriovenous O2 difference), compliance, and wet/dry lung weight were determined.
Pretreatment with NO caused significant increases in pulmonary artery pressure (NO treatment versus NO control and saline control; no significant difference between NO treatment group and OA control group), and did not improve oxygenation in our model.
Contrary to our hypothesis, pretreatment with NO potentiates acute lung injury in our isolated lung model. There was significant exacerbation of pulmonary hypertension and no improvement in oxygenation. Further investigation of the possible deleterious effects of NO in acute lung injury are needed, especially in the early acute phases of this process.
吸入一氧化氮（NO）治疗对成人呼吸窘迫综合征患者肺功能的影响存在争议。我们在油酸（OA）诱导的急性肺损伤的离体兔肺模型中研究了吸入NO对肺功能的影响。我们假设NO会降低肺动脉压并改善氧合。
分离兔心肺组织块，在体内冲洗，收获后立即用全血灌注并用50%氧气（O2）通气。在灌注60分钟期间，每15秒测定一次肺动脉压。在开始输注OA后0、20、40和60分钟，通过对肺静脉流出液进行血气分析来测定氧合。将兔子随机分为四个研究组：生理盐水对照组；OA对照组，接受20分钟的50%OA/乙醇溶液输注；NO治疗组（在输注OA前吸入20 ppm NO）；以及NO对照组，先进行NO（20 ppm）预处理，然后输注生理盐水。测定肺动脉压、氧合（动静脉氧分压差）、顺应性和肺湿/干重。
NO预处理导致肺动脉压显著升高（NO治疗组与NO对照组和生理盐水对照组相比；NO治疗组与OA对照组之间无显著差异），并且在我们的模型中未改善氧合。
与我们的假设相反，在我们的离体肺模型中，NO预处理会加重急性肺损伤。肺动脉高压显著加重，氧合没有改善。需要进一步研究NO在急性肺损伤中可能的有害作用，特别是在该过程的早期急性阶段。
