Humans with severe PE have increased arginase-1 and decreased plasma L-arginine concentrations.[14]
Release of hemoglobin (and ultimately heme), and arginase-1 into the plasma results in binding of nitric oxide and also reduction in L-arginine, respectively, causing a relative reduction in vasodilatory effect.[14,29]
The median values and associated interquartile ranges for hmox-1 and haptoglobin show that patients with PE+TR+ had lower expression of these genes compared with patients who were PE+TR− or PE−
Table 3 shows a significant increase in the median value for the plasma biomarker of hemolysis, arginase-1 in patients with PE+TR+ by pairwise comparison using the Kruskal-Wallis test.
The inverse correlation between hmox-1 expression in circulating leukocytes and the TR jet velocity in patients with acute PE was significant (r2=0.45, p <0.001), but this significance was absent in patients without PE (r2=0.01, P=0.52).
We hypothesize acute moderate to severe PE causes turbulent flow across the tricuspid and pulmonic valves and in the pulmonary tree, causing rupture of a small percentage of red cells in or immediately proximal to or within the pulmonary vascular tree.
The cyclooxygenase-2 gene was not significantly different between groups and had no correlation with the TR jet velocity in patients with PE (R2=0.03).
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.