Zwissler B, Welte M, Habler O, Kleen M, Messmer K
Department of Anesthesia, Ludwig-Maximilians-University Munich, Germany.
J Cardiothorac Vasc Anesth. 1995 Dec;9(6):634-40. doi: 10.1016/s1053-0770(05)80222-8.
Recently, it has been shown that the inhalation of nitric oxide (NO) and of prostacyclin (PGI2) elicits selective pulmonary vasodilation in a canine model of pulmonary hypertension induced by hypoxic pulmonary vasoconstriction. The present study was designed to investigate whether inhaled NO or PGI2-aerosol, respectively, is also effective in decreasing pulmonary artery pressure in a canine model of acute pulmonary microembolism and oleic acid edema.
Prospective, randomized, cross-over design.
University animal research laboratory.
Eight anesthetized, mechanically ventilated dogs (28 +/- 1 kg).
Acute pulmonary microembolization (PME) was induced using glass microbeads (mean diameter: 100 microns) and 0.01 mL/kg of oleic acid. Subsequently, inhaled PGI2 (concentration: 10 micrograms/mL) or NO (50 ppm), respectively, was randomly administered for 15 minutes each and then withdrawn.
Central hemodynamics (heart rate [HR], cardiac output [CO], stroke volume [SV], mean arterial pressure [MAP], systemic vascular resistance [SVR], mean pulmonary artery pressure [PAP], pulmonary vascular resistance [PVR]) and gas exchange (PaO2/FIO2 ratio, intrapulmonary shunt [Qs/Qt], alveolar-arterial oxygen difference, [AaDO2]) were assessed. Measurements were performed at control, after PME, and during administration of PGI2 and NO, respectively. PME induced a significant increase (p < 0.001) of MAP (+9%), PAP (+68%), and PVR (+163%), whereas HR, CO, and SV remained unchanged and lung function deteriorated. Inhalation of NO slightly decreased PAP (-10%; p < 0.05) and PVR (-26%; p < 0.01) and improved AaDO2 and PaO2/FIO2. In contrast, inhalation of PGI2 had no consistent effect on pulmonary vascular tone or gas exchange.
The data demonstrate that inhaled NO may elicit selective pulmonary vasodilation and improve gas exchange in a canine model of pulmonary microembolism and respiratory insufficiency. However, the degree of these effects was relatively small. The aerosolization of PGI2 under conditions of positive-pressure ventilation did not exert a significant vasodilatory effect on pulmonary vessels and did not improve pulmonary gas exchange in this model.
最近的研究表明，在由低氧性肺血管收缩诱导的犬肺动脉高压模型中，吸入一氧化氮（NO）和前列环素（PGI2）可引起选择性肺血管舒张。本研究旨在调查吸入NO或PGI2气雾剂分别在急性肺微栓塞和油酸水肿犬模型中降低肺动脉压是否也有效。
前瞻性、随机、交叉设计。
大学动物研究实验室。
八只麻醉、机械通气的犬（28±1千克）。
使用玻璃微珠（平均直径：100微米）和0.01毫升/千克油酸诱导急性肺微栓塞（PME）。随后，分别随机给予吸入PGI2（浓度：10微克/毫升）或NO（50 ppm）15分钟，然后撤药。
评估中心血流动力学（心率[HR]、心输出量[CO]、每搏量[SV]、平均动脉压[MAP]、全身血管阻力[SVR]、平均肺动脉压[PAP]、肺血管阻力[PVR]）和气体交换（PaO2/FIO2比值、肺内分流[Qs/Qt]、肺泡-动脉氧分压差[AaDO2]）。分别在对照、PME后以及PGI2和NO给药期间进行测量。PME导致MAP（+9%）、PAP（+68%）和PVR（+163%）显著增加（p<0.001），而HR、CO和SV保持不变，肺功能恶化。吸入NO使PAP略有降低（-10%；p<0.05）和PVR降低（-26%；p<0.01），并改善了AaDO2和PaO2/FIO2。相比之下，吸入PGI2对肺血管张力或气体交换没有一致的影响。
数据表明，吸入NO可能在肺微栓塞和呼吸功能不全的犬模型中引起选择性肺血管舒张并改善气体交换。然而，这些作用的程度相对较小。在正压通气条件下PGI2的雾化对肺血管没有显著的血管舒张作用，并且在该模型中没有改善肺气体交换。
