Samama C M, Diaby M, Fellahi J L, Mdhafar A, Eyraud D, Arock M, Guillosson J J, Coriat P, Rouby J J
Département d'Anesthésiologie, Hôpital de la Pitié-Salpêtrière, Université Paris VI, France.
Anesthesiology. 1995 Jul;83(1):56-65. doi: 10.1097/00000542-199507000-00007.
Nitric oxide inhibits platelet adhesion and aggregation in vitro. The aim of this prospective study was to assess the platelet antiaggregating activity of nitric oxide administered to patients with acute respiratory distress syndrome (ARDS) at increasing concentrations.
In six critically ill patients (mean age 37 +/- 16 yr) with ARDS (lung injury severity score > or = 2.2), the lungs were mechanically ventilated with inhaled nitric oxide (1, 3, 10, 30, and 100 ppm) randomly administered. Patients with cardiac dysrhythmias, septic shock, an underlying hemostasis disorder (constitutive or acquired), a platelet count less than 100 Giga/l, or a decreased platelet aggregation and those treated with antiplatelet or anticoagulant agents were excluded. Platelet aggregation was measured without nitric oxide and at each nitric oxide concentration in platelet-rich plasma issued from radial artery. Ivy bleeding time using a horizontal incision was simultaneously performed.
After nitric oxide, a non-dose-dependent but statistically significant decrease in ex vivo platelet aggregation induced by three aggregating agents was observed: adenosine diphosphate = -56 +/- 18%, collagen = -37 +/- 18%, and ristocetin = -45 +/- 18% (P < 0.05). In each individual, Ivy bleeding time remained within normal values measured in healthy volunteers, and variations after nitric oxide did not correlate with changes in platelet aggregation. Simultaneously, arterial oxygenation improved significantly and pulmonary artery pressure decreased significantly.
In patients with ARDS and without preexisting coagulation disorders, the beneficial effects of inhaled nitric oxide on arterial oxygenation and pulmonary circulation are associated with a significant inhibition of platelet aggregation. This antithrombotic effect is not associated with a significant prolongation of the bleeding time.
一氧化氮在体外可抑制血小板黏附和聚集。本前瞻性研究的目的是评估给予急性呼吸窘迫综合征（ARDS）患者不同浓度一氧化氮后其血小板抗聚集活性。
选取6例ARDS重症患者（平均年龄37±16岁，肺损伤严重程度评分≥2.2），随机给予吸入一氧化氮（1、3、10、30和100 ppm）进行机械通气。排除患有心律失常、感染性休克、潜在止血障碍（先天性或后天性）、血小板计数低于100千兆/升、血小板聚集降低的患者以及接受抗血小板或抗凝药物治疗的患者。在无一氧化氮以及在桡动脉采集的富血小板血浆中每种一氧化氮浓度下测量血小板聚集情况。同时采用水平切口法测定Ivy出血时间。
吸入一氧化氮后，观察到由三种聚集剂诱导的体外血小板聚集出现非剂量依赖性但具有统计学意义的降低：二磷酸腺苷=-56±18%；胶原=-37±18%；瑞斯托菌素=-45±18%（P<0.05）。在每个个体中，Ivy出血时间保持在健康志愿者测量的正常范围内，一氧化氮吸入后的变化与血小板聚集的变化无关。同时，动脉氧合显著改善，肺动脉压显著降低。
在无凝血障碍的ARDS患者中，吸入一氧化氮对动脉氧合和肺循环的有益作用与血小板聚集的显著抑制有关。这种抗血栓作用与出血时间的显著延长无关。
