Gries A, Böttiger B W, Dörsam J, Bauer H, Weimann J, Bode C, Martin E, Motsch J
Department of Anesthesiology, University of Heidelberg, Germany.
Anesthesiology. 1997 Feb;86(2):387-93. doi: 10.1097/00000542-199702000-00013.
Inhaled nitric oxide (NO) is reported to prolong bleeding time in animals and humans and to inhibit platelet aggregation in persons with acute respiratory distress syndrome. In pulmonary embolism (PE), inhibition of platelet aggregation appears useful because further thrombus formation may lead to right ventricular dysfunction that results in circulatory failure. In the present study, the effect of inhaled NO on platelet aggregation after acute massive PE was investigated.
After acute massive PE was induced in 25 anesthetized pigs by injecting microspheres, 5, 20, 40, and 80 parts per million inhaled NO were administered stepwise for 10 min each in 11 animals (NO group). In the control group (n = 14). NO was not administered. Adenosine diphosphate-induced initial and maximal platelet aggregation were measured before PE (10), immediately after induction of PE (PE), at the end of each 10-min NO inhalation interval (t10-t40), and 15 min after cessation of NO inhalation (t55) in the NO group, and at corresponding times in the control group, respectively.
Two animals in the control group and one in the NO group died within 10 min after PE induction and were excluded from analysis. Peaking at t40 and t55, respectively, initial (-13 +/- 6%; P < 0.05) and maximal (+44 +/- 17%; P < 0.05) platelet aggregation increased significantly after PE in the control group. In contrast, NO administration after PE led to a significant decrease in initial (maximum decrease, -9 +/- 3% at t40; P < 0.05) and maximal (maximum decrease, -15 +/- 7% at t30; P < 0.05) platelet aggregation. In the NO group, platelet aggregation had returned to baseline levels again at t55. In addition, NO administration significantly decreased mean pulmonary artery pressure and significantly increased end-tidal carbon dioxide concentration and mean systemic blood pressure.
Inhaled NO has a systemic and rapidly reversible inhibitory effect on platelet aggregation after acute massive PE in pigs. This may be beneficial in treating acute massive PE.
据报道，吸入一氧化氮（NO）可延长动物和人类的出血时间，并抑制急性呼吸窘迫综合征患者的血小板聚集。在肺栓塞（PE）中，抑制血小板聚集似乎是有益的，因为进一步的血栓形成可能导致右心室功能障碍，进而导致循环衰竭。在本研究中，研究了吸入NO对急性大面积PE后血小板聚集的影响。
通过注射微球在25只麻醉猪中诱导急性大面积PE后，对11只动物（NO组）分别以百万分之5、20、40和80的剂量逐步给予吸入NO，每次10分钟。在对照组（n = 14）中，不给予NO。分别在PE前（10）、PE诱导后立即（PE）、NO吸入的每个10分钟间隔结束时（t10 - t40）以及NO吸入停止后15分钟（t55）测量NO组中腺苷二磷酸诱导的初始和最大血小板聚集，并在对照组的相应时间进行测量。
对照组中有2只动物和NO组中有1只动物在PE诱导后10分钟内死亡，被排除在分析之外。对照组中，初始（-13±6%；P < 0.05）和最大（+44±17%；P < 0.05）血小板聚集在PE后分别在t40和t55达到峰值并显著增加。相比之下，PE后给予NO导致初始（在t40时最大降低-9±3%；P < 0.05）和最大（在t30时最大降低-15±7%；P < 0.05）血小板聚集显著降低。在NO组中，血小板聚集在t55时再次恢复到基线水平。此外，给予NO显著降低了平均肺动脉压，并显著提高了呼气末二氧化碳浓度和平均体循环血压。
吸入NO对猪急性大面积PE后的血小板聚集具有全身性且快速可逆的抑制作用。这可能对治疗急性大面积PE有益。
