Volume 1 Supplement 1

17th International Symposium on Intensive Care and Emergency Medicine

Open Access

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

  • G Zobel1,
  • S Rödl1,
  • B Urlesberger2,
  • D Dacar3,
  • W Schwinger1 and
  • M Bermoser1
Critical Care19971(Suppl 1):P050

https://doi.org/10.1186/cc56

Published: 1 March 1997

Objective

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

Design

Prospective, randomized, controlled study.

Setting

University research laboratory.

Subjects

Twelve piglets weighing 9 to 13 kg.

Interventions

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.

Conclusions

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.

Table

 

NC

NC

HC-60

HC-60

HC-80

HC-80

iNO (ppm)

0

10

0

10

0

10

MAP (mmHg)

   79 ± 2.9

   81 ± 2.4

   72 ± 2.5

78.3 ± 4.3

74.2 ± 3.0

74.1 ± 3.0

MPAP (mmHg)

28.3 ± 1.8

25.8 ± 1.2

32.6 ± 1.8

  26.7 ± 1.2*

35.1 ± 1.9

  28.5 ± 1.9*

Flow-Pa (l/min)

1.91 ± 0.2

1.99 ± 0.2

1.73 ± 0.1

 1.77 ± 0.1

1.89 ± 0.2

  1.9 ± 0.2

PVR (dyn s/cm5)

684 ± 85

582 ± 99

  928 ± 157

 642 ± 69

  956 ± 142

  685 ± 124

PaO2/FiO2 (torr)

   82 ± 4.2

  143 ± 26*

 100 ± 7.8

  151 ± 19*

96.8± 12

  154 ± 25*

pH

  7.34 ± 0.01

  7.37 ± 0.01

 7.21 ± 0.02

  7.22 ± 0.02

  7.12 ± 0.02

   7.12 ± 0.02

*P< 0.05 NO 0 ppm versus NO 10 ppm, NC = one normocapnia, HC = hypercapnia.

Authors’ Affiliations

(1)
Departments of Pediatrics
(2)
Neonatology
(3)
Cardiac Surgery, University of Graz

Copyright

© Current Science Ltd 1997

Advertisement