Inhaled nitric oxide improves hemodynamics during a venous air infusion (VAI) in dogs

Abstract

Nitrate/nitrite concentrations were unaltered after VAI in dogs. NO therapy attenuated TxA(2) release and improved hemodynamics, but not blood oxygenation, in dogs with a VAI. There were no differences between the responses to 3 ppm and 40 ppm NO.

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

“…In this study, we demonstrate that inhalation of 40 ppm NO causes selective pulmonary vasodilation in animals with sustained pulmonary hypertension due to recurrent pulmonary microembolism. This is consistent with our previous data obtained in the same model (19) and with data from studies in acute pulmonary embolism in animal models (9–14) and in patients (15, 16).…”

“…Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator in patients with the acute respiratory distress syndrome (ARDS), neonates with persistent pulmonary hypertension, and in patients after cardiac surgery (for review see reference 8). Data obtained in animal models of acute PE (9–14) and case reports in humans (15, 16) have suggested a beneficial role of iNO in the treatment of acute PE.…”

Increased expired NO and roles of CO2 and endogenous NO after venous gas embolism in rabbits

“…Inhaled NO has been widely tested as a treatment in PE both in animal models (Bottiger et al 1996;Melot et al 1997;Tanus-Santos et al 1999) and in humans (Capellier et al 1997;Tulleken et al 1998), but with conXicting results. Thus, both beneWcial eVects, like reduced PAP, and negative Wndings have emerged.…”

Protective effects of atorvastatin in rat models of acute pulmonary embolism: Involvement of matrix metalloproteinase-9*

“…It has been shown that activation of the nitric oxide (NO)-cyclic guanosine monophosphate pathway attenuates acute pulmonary embolism-induced hemodynamic derangements (15)(16)(17)(18)(19)(20)(21), maybe through mechanisms including negative modulation of lung MMP-2 and MMP-9 activities after APE (7). Another way to activate the NO-cyclic guanosine monophosphate pathway is by using statins (22)(23)(24).…”