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Inhaled Nitric Oxide versus Inhaled Prostacyclin and Intravenous versus Inhaled Prostacyclin in Acute Respiratory Failure with Pulmonary Hypertension in Piglets

1995; Springer Nature; Volume: 38; Issue: 2 Linguagem: Inglês

10.1203/00006450-199508000-00011

1530-0447

G Zobel, D Dacar, Siegfried Rödl, Ingeborg Friehs,

Neuroscience of respiration and sleep

ABSTRACT: This study was a prospective, randomized design to compare oxygenation and pulmonary hemodynamics between inhaled nitric oxide (NO) and inhaled prostacylcin (PGI2), and between inhaled and i.v. PGI2 in acute respiratory failure with pulmonary hypertension. Acute respiratory failure with pulmonary hypertension was induced in 12 piglets weighing 9–12 kg by repeated lung lavages and a continuous infusion of the stable endoperoxane analogue of thromboxane. Thereafter the animals were randomly assigned either for NO or PGI2 application. All animals were treated with different concentrations of NO or different doses of PGI2 applied i.v. and inhaled in random order. Continuous monitoring included ECG, central venous pressure (CVP), mean pulmonary artery pressure (MPAP), mean arterial pressure (MAP), artertial oxygen saturation (SaO2), and mixed venous oxygen saturation (SvO2) measurements. NO inhalation of 10 ppm resulted in a significant increase in Pao2/fraction of inspired oxygen (FiO2) from 7.8 ± 1.34 kPa to 46.1 ± 9.7 kPa. MPAP decreased significantly from 5.1 ± 0.26 kPa to 3.7 ± 0.26 kPa during inhaled NO of 40 ppm; i.v. infusion of PGI2 slightly increased oxygenation parameters. A significant increase in Pao2/FiO2 up to 32.4 ± 3.1kPa was observed during PGI2 aerosol delivery (p < 0.01); i.v. PGI2 decreased MAP from 11.5 ± 0.39 kPa to 9.8 ± 0.66 kPa (p < 0.05) and MPAP from 5.8 ± 0.53 kPa to 4.5 ± 0.66 kPa, respectively (p < 0.05). PGI2 aerosol delivery significantly decreased the MPAP to 3.7 ± 0.53 kPa (p < 0.05) without influencing the MAP. It was concluded that inhaled NO and inhaled PGI2 act as selective pulmonary vasodilators in acute respiratory failure with pulmonary hypertension resulting in improved oxygenation mainly due to improved mismatch of pulmonary perfusion and ventilation. Intravenous PGI2 improves oxygenation and pulmonary hemodynamics to a lesser extent than aerosolized PGI2 and has the risk of systemic hypotension at a higher dose.