MECONIUM ASPIRATION INDUCES ARDS-LIKE PULMONARY RESPONSE IN LUNGS OF 10-WEEK-OLD PIGS

Citation
H. Soukka et al., MECONIUM ASPIRATION INDUCES ARDS-LIKE PULMONARY RESPONSE IN LUNGS OF 10-WEEK-OLD PIGS, Pediatric pulmonology, 23(3), 1997, pp. 205-211
Citations number
30
Categorie Soggetti
Respiratory System",Pediatrics
Journal title
ISSN journal
87556863
Volume
23
Issue
3
Year of publication
1997
Pages
205 - 211
Database
ISI
SICI code
8755-6863(1997)23:3<205:MAIAPR>2.0.ZU;2-J
Abstract
To investigate whether aspiration of meconium induces a hemodynamic an d histologic pulmonary response similar to that frequently seen in exp erimental acute respiratory distress syndrome, twelve 10-week-old pigs with postnatally adapted lungs were studied. Six 10-week-old pigs rec eived 3 ml/kg 20% human meconium via the endotracheal tube. Six contro l pigs of the same age were given sterile saline. Ventilator settings were adjusted to keep PaO2 above 8 kPa and PaCO2 below 5 kPa. The pulm onary hemodynamic response to aspiration consisted of two separate hyp ertensive components. An initial peak in pulmonary artery pressure (PA P) and pulmonary vascular resistance (PVR) was followed by a progressi ve increase in PAP and PVR in the meconium group, whereas in the salin e group these parameters returned to baseline levels. The distribution of PVR, determined by pulmonary artery occlusion, was characterized b y an increase in the postarterial resistance immediately after meconiu m aspiration and a progressive increase in both arterial and postarter ial resistances during the later phase. On histological examination, m arked neutrophil sequestration was seen in the meconium lungs. In addi tion, lung edema formation was significantly enhanced in the meconium group, as shown by an increased lung wet/dry weight ratio. Thus, mecon ium aspiration resulted in a biphasic pulmonary presser response and s evere pulmonary inflammation. This response resembled that of models o f experimental acute respiratory distress syndrome following diverse t ypes of precipitating insults; this suggests that similar pathophysiol ogic mechanisms are elicited and cause similar pulmonary dysfunction f ollowing different forms of lung injury. (C) 1997 Wiley-Liss, Inc.