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T ElKady

Publications and source records attributed to T ElKady.

2 recordsLinked to original sources

Maternal treatments with corticosteroids and/or T3 change lung volumes and rupture pressures in preterm rabbits.

Pregnant does were treated with betamethasone, T3, the combination of beta-methasone and T3 or vehicle control on days 24 and 25 of gestation. At 26 days gestational age, pressure-volume curves and lung rupture pressures and volumes were measured in the various groups of rabbits randomized to receive saline or surfactant by tracheal injection. Alveolar wash and lung tissue quantities of saturated phosphatidylcholine were comparable across the hormone-treated and control groups. Corticosteroids increased maximal lung volumes more than did T3. Corticosteroids augmented the lung volumes of surfactant-treated lungs more than did T3, and no additive effects on lungs treated with both hormones and surfactant were noted. Both corticosteroids and surfactant decreased lung rupture pressures from 51.7 +/- 4.1 to about 44 cm H2O. T3 decreased lung rupture pressure to 48.9 +/- 3.9 cm H2O and the combination of T3 and corticosteroids resulted in rupture pressures comparable to T3 alone. There were no additive effects of the combined use of T3 and corticosteroids and T3 antagonized the decreased lung rupture pressures caused by corticosteroids. While T3 did not alter the increase in lung volumes noted with corticosteroids, lung structure as assessed by lung rupture was differentially affected by the two hormones.

Animals

Corticosteroids and surfactant increase lung volumes and decrease rupture pressures of preterm rabbit lungs.

We measured the effects of corticosteroids and surfactant individually and in combination on lung pressure-volume relationships, rupture pressures, and rupture volumes. Pregnant does were injected with betamethasone (0.1 mg/kg per day im) or vehicle on days 24 and 25 of gestation, and fetal rabbits were delivered on days 26 and 27. Natural surfactant (50 mg/kg body wt) was instilled intratracheally into half of the lungs after tracheotomy. After nine cycles of inflation with air to 40 cmH2O and deflation, air pressure-volume curves were measured. Then the lungs were filled with air to rupture, and rupture volume and pressure were recorded. Both corticosteroids and surfactant caused an increase in maximal lung volumes (P less than 0.01) and a decrease of lung rupture pressures (P less than 0.01) compared with controls. The effects of corticosteroids plus surfactant on lung volumes were the sum of each effect individually, but rupture pressures were the same as those for corticosteroids or surfactant alone. Surfactant, in addition, caused an increase in lung stability at deflation, an effect that was not evident in the corticosteroid-treated groups. Measurements of saturated phosphatidylcholine in alveolar washes and lung tissue indicated comparable values in the corticosteroid and control groups. We conclude that changes in static properties and rupture pressures presumably reflect changes in lung structure caused by corticosteroids that are independent of a corticosteroid effect on surfactant pool sizes.

Animals