Efeitos do oxido nitrico inalatorio em cães submetidos a embolia aerea

AUTOR(ES)
DATA DE PUBLICAÇÃO

1998

RESUMO

Inhaled nitric oxide (NO) has been used in cases of pulmonary hypertension. Experimental studies have suggested therapeutic effects of NO after pulmonary microembolism. The protective effects of NO inhalation before a massive pulmonary air embolism (PAE) were evaluated in a first study. A second study focused the therapeutic effects of NO inhalation during a venous air infusion (VAI). The thromboxane a release and in vivo NO production were also studied. In the first study NO(3ppm) was initiated in 6 anesthetized mongrel dogs (NO group) but not in the control group (n=7). After 20 min, each dog received a venous air injection of 2.5 ml/kg. Hemodynamicevaluation was performed and blood samples (arterial and mixed venous) were drawn for blood gas analysis before and after NO inhalation, and 5-60 min after the PAE. Three dogs died in the control group vvhereas one dog died in the NO group. PAE decreased both arterial pressure and cardiac output in the control group for- more than 15 min after PAE, while NO¬ treated animals showed only a transient hypotension. NO attenuated the pulmonary hypertension after PAE, as demonstrated by the lower increases in pulmonary artery pressure and vascular resistance in NO-treated animals compared to the controls. These hemodynamic effects of NO were associated with no differences in blood oxygenation. In the second study, anesthetized mongrel dogs received a VAI (0.2 ml.kg-1.min-1) after a baseline (BL) hemodynamic evaluation. Controls (n=8) received no further treatment. After 30 min of VAI (EMB time point), NO 3ppm was initiated in .the NO group (n=7) for 30 min (NO 3 time point), followed by 30 min without NO inhalation (NO O time point). Thereafter NO 40 ppm was inhaled for 30 min (NO 40 time point). Hemodynamic variables were registered and arterial and mixed venous blood samples were drawn for gas analysis, and serum determinations of thromboxane B2 (by ELlSA) and nitrate/nitrite (by HPLC) at BL, EMB, NO 3, NO O and NO 40 time points. Cardiac index increased 24% (p<0.05) and pulmonary vascular resistance index decreased 30% (p<0.05) during both NO inhalation. PaO2 and SaO2 were slightly lower (p<0.05) after NO therapy. Nitrate/nitrite concentrations did not change in the control group. No differences between arterial and mixed venous serum nitrate/nitrite were found. Nitrite concentrations remained below 1 ? M in both groups whereas nitrate concentration increased only at NO 40 (p<0.05). Serum TxB2 increased after 60 min of VAI in the control group (p<0.05), whereas no increase was observed in NO-treated animals. These results indicate that NO attenuates the hemodynamic changes induced by PAE and by a VAI in dogs, without improving pulmonary oxygenation, however. These effects were associated with lower TxA2 concentrations in NO-treated animals and no differences were observed between NO 3 ppm and 40 ppm. Furthermore, endogenous NO release is not impaired afier a VAI in dogs

ASSUNTO(S)

hipertensão pulmonar oxido nitrico cão

ACESSO AO ARTIGO

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