F Xu1, T F Fok, J Yin. 1. Department of Paediatrics, Prince of Wales Hospital, Chinese University of Hong Kong, Shatin, N.T., Hong Kong, China.
Abstract
OBJECTIVE: To provide suitable animal model (hyperoxia-induced premature rat lung damage) for research of bronchopulmonary dysplasia (BPD) and to better understand pathogenesis of BPD and look for effective drugs to prevent and treat BPD. METHODS: Rat litters delivered prematurely at 21-day gestation by hysterotomy. Vigorous resuscitation at birth resulted in a high survival rate. Surfactant and antioxidant enzyme (AOE) system were measured. The model was tested in an experiment of hyperoxia-induced lung injury. RESULTS: Compared to litters delivered spontaneously at term (gestation 22 days), these preterm rats had immature pulmonary surfactant composition with low total phospholipid (x +/- s: 10.09 +/- 1.49 micrograms/mg wet weight vs 12.04 +/- 1.31 micrograms/mg wet weight; P = 0.0367) and phostidylcholine (5.06 +/- 1.82 micrograms/mg wet weight vs 8.28 +/- 2.35 micrograms/mg wet weight; P = 0.0238) levels. The concentrations of AOE enzymes, superoxide dismutase (11.40 +/- 2.04 mu/mg DNA vs 15.78 +/- 1.84 mu/mg DNA; P < 0.01) and catalase (92.81 +/- 62.25 mu/mg DNA vs 412.24 +/- 117.50 mu/mg DNA; P < 0.01) were also significantly lower. Animals exposed to hyperoxia had a significantly higher mortality. Pulmonary edema and histological features of lung damage were observed in the pups exposed to hyperoxia. CONCLUSIONS: The premature rat model is relatively cheap, readily available and has a high survival rate. Pulmonary surfactant and AOE systems are immature. These properties make them a suitable model for the study of acute and chronic lung damage related to prematurity and O2 toxicity.
OBJECTIVE: To provide suitable animal model (hyperoxia-induced premature rat lung damage) for research of bronchopulmonary dysplasia (BPD) and to better understand pathogenesis of BPD and look for effective drugs to prevent and treat BPD. METHODS:Rat litters delivered prematurely at 21-day gestation by hysterotomy. Vigorous resuscitation at birth resulted in a high survival rate. Surfactant and antioxidant enzyme (AOE) system were measured. The model was tested in an experiment of hyperoxia-induced lung injury. RESULTS: Compared to litters delivered spontaneously at term (gestation 22 days), these preterm rats had immature pulmonary surfactant composition with low total phospholipid (x +/- s: 10.09 +/- 1.49 micrograms/mg wet weight vs 12.04 +/- 1.31 micrograms/mg wet weight; P = 0.0367) and phostidylcholine (5.06 +/- 1.82 micrograms/mg wet weight vs 8.28 +/- 2.35 micrograms/mg wet weight; P = 0.0238) levels. The concentrations of AOE enzymes, superoxide dismutase (11.40 +/- 2.04 mu/mg DNA vs 15.78 +/- 1.84 mu/mg DNA; P < 0.01) and catalase (92.81 +/- 62.25 mu/mg DNA vs 412.24 +/- 117.50 mu/mg DNA; P < 0.01) were also significantly lower. Animals exposed to hyperoxia had a significantly higher mortality. Pulmonary edema and histological features of lung damage were observed in the pups exposed to hyperoxia. CONCLUSIONS: The premature rat model is relatively cheap, readily available and has a high survival rate. Pulmonary surfactant and AOE systems are immature. These properties make them a suitable model for the study of acute and chronic lung damage related to prematurity and O2toxicity.
Authors: Vivek Balasubramaniam; Sharon L Ryan; Gregory J Seedorf; Emily V Roth; Thatcher R Heumann; Mervin C Yoder; David A Ingram; Christopher J Hogan; Neil E Markham; Steven H Abman Journal: Am J Physiol Lung Cell Mol Physiol Date: 2009-12-11 Impact factor: 5.464