Pulmonary Arterial Hypertension and Endothelial Dysfunction Is Linked to NADPH Oxidase-Derived Superoxide Formation in Venous Thrombosis and Pulmonary Embolism in Mice
IVC ligation has no effect on pulmonary hemodynamics, while sublethal acute pulmonary embolism induced by intravenous thrombin injection results in pulmonary hypertension and right ventricular dysfunction. (a) left subpanel: B-mode imaging in parasternal short-axis view shows normal morphology of cardiac left and right ventricles (LV and RV, resp.), while noninvasive assessment of pulmonary arterial/right ventricular systolic pressure (RVSP) by measurement of pulmonary arterial acceleration time (PAT) did not reveal an increase in RVSP ((c) left subpanel). (b) left subpanel: representative PW-Doppler tracings 24 h after induction of IVC-thrombus formation by IVC ligation. Immediately after induction of sublethal acute PE by intravenous thrombin injection, cardiac imaging revealed RV enlargement ((a) right subpanel) correlating to a significantly decreased PAT indicating a significant increase in RVSP ((c) right subpanel, results are presented as PAT (ms) and as calculated RVSP (mmHg), with a cutoff of 21 ms (PAT)/32 mmHg (RVSP) between normal and elevated PAP, with the grey area indicating the regions of elevated PAP ). (b) right subpanel: representative tracings. IVCL: IVC ligated mice. 5 animals per group; data are presented as mean and SEM. t-test.