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

Abstract

Venous gas embolism (VGE) is a feared complication in diving, aviation, surgery and trauma. We hypothesized that air emboli in the lung circulation might change expired nitric oxide (FeNO). A single intravenous infusion of air was given (100 mul kg(-1)) to three groups of anaesthetized mechanically ventilated rabbits: (A) one with intact NO production, (B) one with intact NO production and where end-tidal CO(2) was controlled, and (C) one with endogenous NO synthesis blockade (L: -NAME, 30 mg kg(-1)). Air infusions resulted in increased FeNO of the control group from 20 (4) [mean (SD)] ppb to a peak value of 39 (4) ppb within 5 min (P < 0.05), and FeNO was still significantly elevated [27 (2) ppb] after 20 min (P < 0.05). Parallel to the NO increase there were significant decreases in end-tidal CO(2 )(ETCO(2)) and mean arterial pressure and an increase in insufflation pressure. In group B, when CO(2) was supplemented after air infusion, NO was suppressed (P = 0.033), but was still significantly elevated compared with pre-infusion control (P < 0.05). In group C, all animals died within 40 min of air infusion whereas all animals in the other groups were still alive at this time point. We conclude that venous air embolization increases FeNO, and that a part of this effect is due to the concomitant decrease in ETCO(2). Furthermore, an intact NO production may be critical for the tolerance to VGE. Finally, FeNO might have a potential in the diagnosis and monitoring of pulmonary gas embolism.

Aminoguanidine produces beneficial haemodynamic effects in a canine model of acute pulmonary thromboembolism

“…In line with previous reports (Emerson et al. 1999, Agvald et al. 2006), our results indicate that endogenous NO protects against the pulmonary hypertension and the mortality associated with acute pulmonary embolism, although the study by Agvald et al.…”

“…Whereas endogenous NO production protects against the mortality associated with pulmonary embolization (Emerson et al. 1999, Agvald et al. 2006), we found that iNOS‐derived NO produces unfavourable effects.…”

“…Conversely, there are only two experimental studies showing that inhibition of endogenous NO production with the nonspecific NOS inhibitor l ‐NAME increases the mortality associated with APT (Emerson et al. 1999) or gas embolism (Agvald et al. 2006).…”

Venous Air Embolism

“…111 A study in rabbits suggests that any hope of a favorable physiological response to VAE requires an intact endogenous production of nitric oxide, as blockade of this system resulted in universal fatalities. 112 In dogs, antagonism of endothelin-1, a vasoactive mediator released after pulmonary embolism, attenuated both the decrease in mean arterial pressure and the increase in pulmonary vascular resistance seen after VAE. 87 Anecdotally, inhaled epoprostenol has been used successfully after carbon dioxide embolism, resulting in prompt normalization of PAP.…”

Treatment with new organic nitrites in pulmonary hypertension of acute experimental pulmonary embolism

“…NO is a vasodilator in the pulmonary circulation 4 and we found that the fraction of NO in exhaled gas (FENO) increased in acute PE and that endogenous NO production was protective in two models of experimental PE. 5,6 The NO donors nitroglycerin and sodium nitroprusside have shown some beneficial effects in animal models of PE, but the vasodilation was more pronounced in the systemic circulation and nitroglycerin may also impair the gas exchange, thereby limiting the applicability of these drugs in acute PE. 7,8 Furthermore, sildenafil, inorganic nitrite and a nitric oxide-releasing aspirin have shown beneficial effects in animal models of acute PE.…”