Abstract
To investigate the correlation of inhaled nitric oxide (NO) on plasma levels of cardiac troponin I (cTnI) and von Willebrand factor (vWF), glycoprotein (GP) IIb/IIIa, granule membrane protein 140 (GMP-140) in rabbits with acute massive pulmonary embolism (PE). Thirty apanese white rabbits were divided into 3 groups, thrombus were injected in model group (n = 10), NO were inhalated for 24 h after massive PE in NO group (n = 10), saline were injected in control group (n = 10). The concentrations of vWF, GP IIb/IIIa, GMP-140 and cTnI were tested at 4, 8, 12, 16, 20, and 24 h, Correlation analyses were conducted between cTnI and vWF, GP IIb/IIIa, and GMP-140 by Pearson's correlation. The concentration of cTnI and vWF, GP IIb/IIIa, and GMP-140 was increased in the model group, compared to control group. In the inhaled group, the concentrations of cTnI, vWF, GP IIb/IIIa, and GMP-140 were reduced compared to model group. There was a positive correlation between cTnI and vWF, GP IIb/IIIa, and GMP-140. Inhaled nitric oxide can lead to a decrease in levels of cardiac troponin I, von Willebrand factor, glycoprotein, and granule membrane protein 140, after an established myocardial damage, provoked by acute massive pulmonary embolism.
Highlights
The mortality rate of acute massive pulmonary thromboembolism was about 30%3-4, which was very high[1,2], in patients with shock or heart failure, so the risk of mortality should be assessed as early as possible to maintain more effective treatments[5,6,7]
Right ventricle dysfunction in patients with hemodynamic instability are included in high-risk group[5], in which cardiac troponin is increased in the pulmonary thromboembolism with heart failure
The rabbits were randomly divided into three groups: model group (n = 10), the thrombus was made of autologous venous blood and inject through the jugular vein, establish massive pulmonary thromboembolism model; inhaled group (n = 10), the rabbits inhaled nitric oxide (NO)(20ppm) for 24 h at 2 h after modeling; control group (n = 10), NS injected through jugular vein into the rabbits
Summary
The mortality rate of acute massive pulmonary thromboembolism was about 30%3-4, which was very high[1,2], in patients with shock or heart failure,, so the risk of mortality should be assessed as early as possible to maintain more effective treatments[5,6,7]. Right ventricle dysfunction in patients with hemodynamic instability are included in high-risk group[5], in which cardiac troponin is increased in the pulmonary thromboembolism with heart failure. These factors indicate myocardial damage and poor prognosis but are not well-understood[8,9]. In the past 20 years, NO has become one of the most important signaling molecules in the cardiovascular system and is considered as a heart protection mediator[17]
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