The effects of inhaled NO on plasma vasoactive factor and CTnI level in rabbits with acute massive pulmonary embolism

Abstract Purpose: To investigate changes in the plasma concentrations of cardiac troponin I (CTnI), thromboxane A2 (TXA2), prostaglandin I2 (PGI2) and endothelin-1 (ET-1) in rabbits with massive pulmonary embolism (AMPE) and the impact of nitric oxide inhalation (NOI) on these indices. Methods: A total of 30 Japanese rabbits were used to construct an MPE model and were divided into 3 groups equally (n=10), including an EXP group (undergoing modeling alone), an NOI group (receiving NOI 2 h post-modeling) and a CON group (receiving intravenous physiological saline). Results: In the model group, plasma concentration of CTnI peaked at 16 h following modeling (0.46±0.10 µg/ml) and significantly decreased following NOI. Plasma levels of TXB2, PGI2 and ET-1 peaked at 12, 16 and 8 h following modeling, respectively, and significantly decreased at different time points (0, 2, 4, 8, 12, 16, 20 and 24 h) following NOI. A significant correlation was observed between the peak plasma CTnI concentration and peak TXB2, 6-keto prostaglandin F1α and ET-1 concentrations in the model and NOI groups. Conclusion: Increases in plasma TXA2, PGI2 and ET-1 levels causes myocardial damage in a rabbit model of AMPE; however, NOI effectively down regulates the plasma concentration of these molecules to produce a myocardial-protective effect.

摘要 目的：探讨大面积肺栓塞（massive pulmonary embolism, AMPE）家兔血浆心肌肌钙蛋白I（cardiac troponin I, CTnI）、血栓素A2（thromboxane A2, TXA2）、前列腺素I2（prostaglandin I2, PGI2）及内皮素-1（endothelin-1, ET-1）浓度变化，以及吸入一氧化氮（nitric oxide inhalation, NOI）对上述指标的影响。
方法：共选用30只日本家兔构建大面积肺栓塞模型，将其均分为3组（n=10），分别为单纯造模组（EXP组）、造模后2小时给予吸入一氧化氮治疗组（NOI组）及静脉输注生理盐水对照组（CON组）。
结果：单纯造模组家兔的血浆CTnI浓度于造模后16小时达峰值（0.46±0.10 µg/ml），经NOI治疗后其浓度显著降低。造模组家兔血浆血栓素B2（thromboxane B2, TXB2）、PGI2及ET-1浓度分别于造模后12、16及8小时达峰值，经NOI治疗后，于给药后不同时间点（0、2、4、8、12、16、20及24小时）其浓度均显著下降。单纯造模组与NOI组家兔的血浆CTnI峰值浓度与TXB2、6-酮前列腺素F1α及ET-1峰值浓度均存在显著相关性。
结论：在AMPE家兔模型中，血浆TXA2、PGI2及ET-1水平升高可引发心肌损伤；而吸入一氧化氮可有效下调上述分子的血浆浓度，进而发挥心肌保护作用。