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Meconium aspiration induces ARDS‐like pulmonary response in lungs of ten‐week‐old pigs
Author(s) -
Soukka Hanna,
Rautanen Markku,
Halkola Lauri,
Kero Pentti,
Kääpä Pekka
Publication year - 1997
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/(sici)1099-0496(199703)23:3<205::aid-ppul6>3.0.co;2-m
Subject(s) - medicine , ards , meconium aspiration syndrome , meconium , lung , respiratory disease , anesthesia , pregnancy , fetus , biology , genetics
To investigate whether aspiration of meconium induces a hemodynamic and histologic pulmonary response similar to that frequently seen in experimental acute respiratory distress syndrome, twelve 10‐week‐old pigs with postnatally adapted lungs were studied. Six 10‐week‐old pigs received 3 ml/kg 20% human meconium via the endotracheal tube. Six control pigs of the same age were given sterile saline. Ventilator settings were adjusted to keep PaO 2 above 8 kPa and PaCO 2 below 5 kPa. The pulmonary hemodynamic response to aspiration consisted of two separate hypertensive components. An initial peak in pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) was followed by a progressive increase in PAP and PVR in the meconium group, whereas in the saline group these parameters returned to baseline levels. The distribution of PVR, determined by pulmonary artery occlusion, was characterized by an increase in the postarterial resistance immediately after meconium aspiration and a progressive increase in both arterial and postarterial resistances during the later phase. On histological examination, marked neutrophil sequestration was seen in the meconium lungs. In addition, lung edema formation was significantly enhanced in the meconium group, as shown by an increased lung wet/dry weight ratio. Thus, meconium aspiration resulted in a biphasic pulmonary pressor response and severe pulmonary inflammation. This response resembled that of models of experimental acute respiratory distress syndrome following diverse types of precipitating insults; this suggests that similar pathophysiologic mechanisms are elicited and cause similar pulmonary dysfunction following different forms of lung injury. Pediatr. Pulmonol. 1997; 23:205–211 © 1997 Wiley‐Liss, Inc.