Abstract
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. 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). 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. 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.
Highlights
Acute massive pulmonary embolism (AMPE) is associated with high early mortality[1,2] of ~30%, in patients who present with concomitant shock and heart failure[3,4]
The right ventricular wall was thinner in rabbits from the EXP group compared with those in the nitric oxide inhalation (NOI) group (Figure 1E and F)
Increased concentrations of ET-1 and thromboxane A2 (TXA2), as well as the balance maintained between TXA2 and prostaglandin I2 (PGI2), may serve a key role in the increased resistance in pulmonary circulation, pulmonary hypertension, and myocardial damage. This present study demonstrated that NOI is able to significantly reduce plasma concentrations of TXA2, PGI2, ET-1 and cardiac troponin I (CTnI) in rabbits with AMPE
Summary
Acute massive pulmonary embolism (AMPE) is associated with high early mortality[1,2] of ~30%, in patients who present with concomitant shock and heart failure[3,4]. Early assessment of mortality risk as well as early and effective treatment is recommended for the successful management of AMPE5-7. Patients presenting with right ventricular (RV) dysfunction and hemodynamic instability are in the high-risk group[5]. The mechanisms responsible for myocardial damage in patients with PE in the high-risk group are unclear[5,6]; when patients present with concomitant heart failure, they typically have elevated cardiac troponin I (CTnI) levels[7,8]. Elucidating the mechanisms and factors that precipitate myocardial damage in patients with PE may be useful for predicting and improving patient prognoses
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