Effects of oxygen and nitric oxide inhalation in a porcine model of recurrent microembolism

Abstract

We conclude that both O2 and iNO are selective pulmonary vasodilators in a porcine model of sustained pulmonary hypertension following recurrent pulmonary microembolism and, therefore, may be useful in the treatment not only in the acute phase of pulmonary embolism but also later in the time course of the disease.

Hemodynamic effects of sildenafil interaction with a nitric oxide donor compound in a dog model of acute pulmonary embolism

“…While it is generally accepted that selective pulmonary vasodilators may attenuate APEinduced pulmonary hypertension, only inhaled NO or intravenous sildenafil, a specific phosphodiesterase type 5 (PDE5) inhibitor (Webb et al, 2000) which increases tissue concentrations of cyclic guanosine 3′,5′-monophosphate (cGMP), produced selective pulmonary vasodilation during experimentally induced APE (Bottiger et al, 1996;Dias-Junior et al, 2005a,b;Smulders, 2000). Moreover, we and others have demonstrated that inhaled nitric oxide (NO) consistently attenuates the pulmonary hypertension found in different animal models of APE (Bottiger et al, 1996;Tanus-Santos et al, 1999a,b;Weimann et al, 2000). In addition, L-arginine, which is substrate for NO synthesis, attenuated APE-induced pulmonary hypertension in an isolated rat lung model of APE through mechanisms involving increased NO synthesis (Souza-Costa et al, 2005).…”

Riociguat, sildenafil and inhaled nitric oxide reduces pulmonary vascular resistance and improves right ventricular function in a porcine model of acute pulmonary embolism

“…Our study therefore adds novel insights to the growing body of preclinical data, suggesting that NO-sGC-cGMP stimulation may be safe and beneficial in intermediate-risk pulmonary embolism. 3,[14][15][16][17][18][19][20][21][22][23] While case reports and smaller series also show promising effects, [6][7][8][9][10][11][12] the first, recently published, randomized clinical trial failed to reduce the combined, primary end point of normalization of RV function, evaluated by echocardiography and biomarkers of RV strain. 13 Inhaled NO did, however, attenuate RV dilatation and hypokinesia, indicating a beneficial effect as seen in the present study.…”

“…[6][7][8][9][10][11][12][13] Experimental data are promising but studies have been performed in models of acute pulmonary embolism using artificial plastic spheres or models of nonpulmonary embolism-related or chronic pulmonary hypertension. 3,[14][15][16][17][18][19][20][21][22][23] It is currently unknown whether the pulmonary vasodilatory effects found in these studies translate to the more physiological setting of acute pulmonary embolism caused by larger thromboemboli.…”

Hemodynamic Benefits of Matrix Metalloproteinase-9 Inhibition by Doxycycline During Experimental Acute Pulmonary Embolism

“…(2) Emb group (n = 8), which received 200 µL of saline IV followed 10 minutes later by a 200 µL IV injection of a suspension of 300 µm microspheres (Sephadex G50, Pharmacia Biotech, Frieburg, Germany; 9 mg/kg) 15 ; (3) Doxy group (n = 4), which received 200 µL of a doxycycline solution (30 mg/kg) 16 IV followed 10 minutes later by an injection of 200 µL of saline IV; (4) Doxy + Emb group (n = 8), which received the same dose of doxycycline described in the Doxy group followed 10 minutes later by the same amount of microspheres described in Emb group.…”