Silvera F.E.,Area Basica |
Blasina M.F.,Area Basica |
Blasina M.F.,Institute Investigaciones Biologicas Clemente Estable |
Vaamonde L.,Area Basica |
And 6 more authors.
Brazilian Journal of Medical and Biological Research | Year: 2011
Meconium aspiration syndrome causes respiratory failure after birth and in vivo monitoring of pulmonary edema is difficult. The objective of the present study was to assess hemodynamic changes and edema measured by transcardiopulmonary thermodilution in low weight newborn piglets. Additionally, the effect of early administration of sildenafil (2 mg/kg vo, 30 min after meconium aspiration) on this critical parameter was determined in the meconium aspiration syndrome model. Thirty-eight mechanically ventilated anesthetized male piglets (Sus scrofa domestica) aged 12 to 72 h (1660 ± 192 g) received diluted fresh human meconium in the airway in order to evoke pulmonary hypertension (PHT). Extravascular lung water was measured in vivo with a PiCCO monitor and ex vivo by the gravimetric method, resulting in an overestimate of 3.5 ± 2.3 mL compared to the first measurement. A significant PHT of 15 Torr above basal pressure was observed, similar to that of severely affected humans, leading to an increase in ventilatory support. The vascular permeability index increased 57%, suggesting altered alveolocapillary membrane permeability. Histology revealed tissue vessel congestion and nonspecific chemical pneumonitis. A group of animals received sildenafil, which prevented the development of PHT and lung edema, as evaluated by in vivo monitoring. In summary, the transcardiopulmonary thermodilution method is a reliable tool for monitoring critical newborn changes, offering the opportunity to experimentally explore putative therapeutics in vivo. Sildenafil could be employed to prevent PHT and edema if used in the first stages of development of the disease.
Martell M.,Area Basica |
Blasina F.,Area Basica |
Tellechea S.,Area Basica |
Tellechea S.,Institute Investigaciones Clemente Estable |
And 6 more authors.
Revista Chilena de Pediatria | Year: 2011
Pulmonary hypertension (HTP) is a frequently pathological situation of maladaptation to the extratuerine life in newborns. Hypoxia and acidosis are key factors capable of evoking the referred situation and can also act as a perpetuator factor of it. Objectives: To evaluate the effect of inhaled nitric oxide (iNO) on pulmonary vascular response to hypoxia and acidosis in newborn pigs. Material and Methods: we performed a series of experimental interventions in newborn pigs, sedated, anesthetized and mechanical ventilation. The experimental protocol was to induce hypoxia in a controlled and progressive (FiO2 from 0.21 (baseline) to 0.14, 0.10 or 0.08, mixing nitrogen with air), between 6 and 10 minutes, evaluating the hemodynamic response. Stabilized response to hypoxia plateau elevation in pulmonary artery pressure (PAP) and systemic administered iNO at 20 ppm. By infusion of HCl 0.1 N i/v was stable at different pH values which were reiterated in this series of experiments. Results: we found that the decrease in FiO2 (below 0,21) produces a fall in saturation and an immediate increase in PAP at different pH and an ERA of iNO for the PAP down near 70%. However, at lower pH, the presence of acidosis produces a basal level of PAP high relative to pH 7.4, which does not descend iNO. As PH developed at different FiO2 was confirmed that the elevation of the PAP is gradually higher. Conclusion: experimental research in newborn pigs shows that the short-term hypoxic events generate HTP and instability on systemic hemodynamics. Similarly acidosis induces an increase in baseline PAP in this experimental model. Under these conditions the application of iNO decreases the PAP effectively without altering systemic hemodynamics. Its action is more effective at normal pH than in acidosis.