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Effects of inhaled nitric oxide during permissive hypercapnia in acute respiratory failure in piglets


To evaluate gas exchange and pulmonary hemodynamic data during permissive hypercapnia (PHC) and inhaled nitric oxide (NO) in acute respiratory failure.


Prospective, randomized, controlled study.


University research laboratory.


Twelve piglets weighing 9 to 13 kg.


After induction of anesthesia, tracheostomy and controlled mechanical ventilation animals were instrumented with two central venous catheters, a pulmonary artery and a femoral artery catheter, and an ultrasonic flow probe on the pulmonary artery and the ascending aorta. Acute respiratory failure was induced by the infusion of oleic acid (0.1 ml/kg) and repeated lung lavages with 0.9% NaCl (20 ml/kg). The protocol consisted of three randomly assigned periods with different PaCO2 levels (NC = PaCO2 40 torr, PHC-60 = PaCO2 60 torr, PHC-80 = PaCO2 80 torr). Tidal volume was reduced to induce hypercapnia, pH was not corrected. At each PaCO2 period the animals were ventilated with and without inhaled NO.

Measurements and results

Continuous monitoring included ECG, CVP, MPAP, MAP, SaO2 and SvO2 measurements. In addition, the blood flow in the pulmonary artery and aorta was measured continuously. Data are given as mean ± SEM. For statistical comparison ANOVA for repeated measures was used.


The pressure but not the flow in the pulmonary artery increased rapidly during acute permissive hypercapnia. Inhaled NO significantly reduced the pulmonary hypertension induced by acute permissive hypercapnia but did not influence the flow through the pulmonary artery. Inhaled NO significantly improved oxygenation in this model of ARF both during normocapnia and permissive hypercapnia.


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Zobel, G., Rödl, S., Urlesberger, B. et al. Effects of inhaled nitric oxide during permissive hypercapnia in acute respiratory failure in piglets. Crit Care 1 (Suppl 1), P050 (1997).

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