A comparison of two protocols testing the effects of prenatal steroids on diaphragm development in guinea pigs


Meeting Abstract

P1.43  Thursday, Jan. 3  A comparison of two protocols testing the effects of prenatal steroids on diaphragm development in guinea pigs WEIGAND, K.L.**; ALEXANDER, R.E.; DEAROLF, J.L.; Hendrix College, Conway, AR; Hendrix College, Conway, AR; Hendrix College, Conway, AR oberle@hendrix.edu

Glucocorticoids are naturally present at increased levels during the late period of gestation and stimulate lung development, including increasing surfactant production. Based on this characteristic, women at risk for preterm delivery are given steroids to induce rapid development of the lungs of their fetuses and decrease the risk of mortality. However, steroid exposure has been shown to cause atrophy in the diaphragm muscle and a decreased percentage of type II fibers in the hindlimb muscles of fetal sheep. In order to assess the effects of prenatal steroids on diaphragm development, two injection protocols were compared in guinea pigs. Both protocols required intramuscular injections of betamethasone in treated females and sterile water for control females. Injection volumes were based on the female�s mass (0.5 mg/kg) at the time of each pair of injections. One protocol called for two injections, 24 hours apart, at 70% gestation. The other protocol required three courses of two injections, each set of two at 24 hour intervals, administered at 65%, 75% and 85% gestation. Females were euthanized by CO2 inhalation and an overdose of sodium pentobarbital was administered to all fetuses. Fetal tissue was immediately collected and frozen. The diaphragm samples were processed using myosin-ATPase histochemistry to determine their fiber-type composition. If the fiber diameters or percentage of type II fibers is decreased in treated fetuses of either protocol, it will suggest prenatal steroids have a detrimental effect on diaphragm development. The functional consequences of these changes may be marked in human neonates exposed to prenatal steroids, causing them to be unable to respond to ventilatory challenges as well as unexposed neonates.

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