Simulated transport alters surfactant homeostasis and causes dose-dependent changes in respiratory function in neonatal Sprague-Dawley rats.
Forces transmitted to the neonate as a consequence of accelerations during transport have been associated with adverse neonatal outcomes including broncho-pulmonary dysplasia. In this study, we sought to determine the relationship between the duration of transport and respiratory performance in the rat model.



Four groups of Sprague-Dawley rat pups (10-12 pups/groups) were exposed to simulated medical transport on postnatal day of life 11 or 12. Each group was exposed to an average impulse of 27.4 m/s(2)/min for 0, 30, 60 or 90 min. During the exposure periods, impulse was monitored by computerized sampling using a digital accelerometer. Post-exposure, animals were immediately prepared, placed on mechanical ventilation and analyzed for elastance, tissue damping, airway resistance, ratio of damping to elastance (eta), hysteresivity, and inertance at positive end expiratory pressures (PEEPs) of 0, 3 and 6 cm(3) of H(2)O. Total phospholipid content and surfactant proteins A, B, and C mRNA levels in broncho-alveolar lavage fluid and lung tissue were obtained.



Increased transport time resulted in a significant step-wise increase in airway resistance at all levels of PEEP (P<0.01). Static compliance decreased significantly after 60 min at PEEPs of 3 and 6 cm H(2)O (P<0.01). Eta significantly decreased with greater transport time at a PEEP of 6 cm H(2)O (P<0.05). Tissue damping increased with duration of transport time across all PEEP levels, but only exhibited statistical significance at a PEEP of 0 cm H(2)O (P<0.05). No differences were seen in hysteresivity or inertance. Compared with controls, transport was associated with significant reductions in total phospholipid content and mRNA levels of surfactant proteins B and C.



Rat pups experienced significant deterioration of respiratory function with increasing duration of simulated transport.
Shah
Shetal
S
Division of Neonatology, Department of Pediatrics, State University of New York at Stony Brook, Stony Brook, New York, NY, USA. shetaldoc@hotmail.com
Hudak
Joseph
J
Gad
Ashraf
A
Cohen
J Craig
JC
Chander
Avinash
A
D000054:Acceleration / Q000009:adverse effects*; D055371:Acute Lung Injury / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D000403:Airway Resistance; D000818:Animals; D000831:Animals, Newborn; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D001997:Bronchopulmonary Dysplasia / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D004548:Elasticity; D005260:Female; D006706:Homeostasis; D006801:Humans; D007231:Infant, Newborn; D008170:Lung Compliance; D008297:Male; D023421:Models, Animal; D010743:Phospholipids / Q000378:metabolism; D011175:Positive-Pressure Respiration; D037661:Pulmonary Surfactant-Associated Proteins / Q000235:genetics / Q000502:physiology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012143:Respiratory Physiological Phenomena; D014187:Transportation of Patients
D010743:Phospholipids; D037661:Pulmonary Surfactant-Associated Proteins; D012333:RNA, Messenger