Inhaled Nitric Oxide Selectively Decreases Pulmonary Artery Pressure and Pulmonary Vascular Resistance Following Acute Massive Pulmonary Microembolism in Piglets

Effects of levosimendan on acute pulmonary embolism-induced right ventricular failure*

“…While the current treatment of acute pulmonary embolism is focused on removing the mechanical obstruction of the pulmonary vessels (24), pharmacologic interventions to reverse pulmonary vasoconstriction are now being considered as potentially effective (20). Pulmonary vasodilators have been tested in animal models, but only nitric oxide, sildenafil, and inhibitors of thromboxane A 2 synthase were found to dilate pulmonary vessels without altering gas exchange (11,20,25,26). Recent experimental studies showed that an acute increase in PA pressure is associated with a persistent reduction in RV contractility, in proportion to the increase in systolic wall stress (17,18,27,28).…”

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

“…(Dias-Junior et al, 2005a,b) This model of APE is very similar to that previously reported. (Bottiger et al, 1996) Hemodynamic evaluation was performed 15 and 30 min (15E and 30E time points, respectively) after the APE was induced, and the animals were randomly assigned to one of five experimental groups: (1) the dogs in DETA + Sild group (n = 8) received a bolus injection of 1μMol kg − 1 of diethylenetriamine nonoate (DETA-NO, Caymann Chemical, Ann Arbor, MI, USA) (Lam et al, 2003) infused intravenously in 15 min) followed by a 30 min infusion of sildenafil 0.3 mg kg − 1 h − 1 (Pfizer, São Paulo, Brazil) (Dias-Junior et al, 2005b;Yoo et al, 2002); (2) another group received only bolus injection of 1μMol kg − 1 of DETA (DETA group; n = 9) infused intravenously in 15 min followed by a 30min infusion of the same volume of saline; (3) those dogs in Sild group (n = 8) received only saline infused intravenously in 15min followed by a 30min infusion of 0.3 mg kg − 1 of sildenafil; (4) those dogs in the Control group (n = 8) received the same volume of saline; (5) finally, a group of Sham operated animals (n = 3) received only saline infusions. In the present study, we used the intravenous route of administration because it is seems to be the most convenient route.…”

“…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).…”

Isquemia pulmonar embólica: aspectos clínicos e experimentais

“…A embolia pulmonar com ar, em ratos, pode produzir obstrução da microvasculatura e levar a alterações na permeabilidade, liberação de mediadores e injúria de envolvimento leucocitário, com conseqüente elevação da pressão arterial pulmonar 61 . Através da embolia experimental tem se estudado as variações na resistência vascular e na pressão arterial pulmonares 62 , alterações de troca gasosa 54 , alterações no parênquima pulmonar, como edema 17 , hemorragia intraalveolar 56 ou infarto 63 . Estudo realizado em cães estabeleceu o papel dos fatores humorais liberados pela agregação plaquetária na embolia pulmonar, excluindo nesse modelo agudo a participação dos fatores mecânico e reflexo, como a vasoconstricção, na produção das alterações presentes de queda no fluxo capilar, de aumento da resistência vascular pulmonar, edema intersticial, atelectasia e hemorragia 56 .…”