Pulmonary Arterial Hypertension and Endothelial Dysfunction Is Linked to NADPH Oxidase-Derived Superoxide Formation in Venous Thrombosis and Pulmonary Embolism in Mice

Figure 2

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 [5]). (b) right subpanel: representative tracings. IVCL: IVC ligated mice. 5 animals per group; data are presented as mean and SEM. t-test.