Am J Perinatol 1985; 2(2): 101-107
DOI: 10.1055/s-2007-999924
ORIGINAL ARTICLE

© 1985 by Thieme Medical Publishers, Inc.

Asphyxia and Hyaline Membrane Disease in Neonatal Monkeys

Jack R. Hessler1 , Gonzalo Mantilla2 , Barry V. Kirkpatrick3 , William H. Donnelly4 , Sidney Cassin5 , Donald V. Eitzman6
  • 1Department of Physiology and Biophysics, University of Tennessee Center for the Health Sciences, Memphis, Tennessee
  • 2Department of Pediatrics, University Medical Center, Jacksonville, Florida
  • 3Department of Pediatrics, Medical College of Virginia, Richmond, Virginia
  • 4Department of Pathology, J. Hillis-Miller Health Center, University of Florida, Gainesville, Florida
  • 5Department of Physiology, J. Hillis-Miller Health Center, University of Florida, Gainesville, Florida
  • 6Department of Pediatrics, J. Hillis-Miller Health Center, University of Florida, Gainesville, Florida
Further Information

Publication History

Publication Date:
04 March 2008 (online)

ABSTRACT

An animal model for studying the relationship between perinatal asphyxia and hyaline membrane disease (HMD) is described. The HMD developed in these Macaca mulatta (rhesus) and M. arctoides (stump tail) monkeys was clinically, physiologically, and histologically similar to that seen in human infants. The monkeys were delivered by cesarean section at a gestational age of 85-91% of term when surfactant, though present, was less than mature levels. Asphyxia at birth proved to be an important factor in disease development. Five minutes of asphyxia immediately before the first breath greatly increased the incidence and severity of HMD when compared to nonasphyxiated controls of a similar gestational age. Amniotic fluid L/S ratios did not differ significantly in the asphyxiated and control groups but data based on static pressure-volume studies of the excised lungs indicated that the surfactant activity of the asphyxiated group was significantly less. Lung maturity with regard to surfactant production appears to be a critical factor. The data from these experiments, together with data cited in the literature, strongly suggest that the lung and its surfactant system is most vulnerable to hypoxia and/or acidosis during the early stages of surfactant production. The asphyxiated non-human primate model used here should prove valuable for studying the pathogenesis of HMD and especially for futher clarifying the relationship between perinatal asphyxia and HMD.