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The effects of alpha adrenergic receptor stimulation, using epinephrine, on lung fluid production in in vitro preparations of lung from fetal guinea pigs (Cavia porcellus) Doe, Sam


This study examined the effects of epinephrine on fluid production and reabsorption by fetal guinea pig lungs. Catecholamine levels in the fetus have been found to increase significantly near term and epinephrine has been proposed to play a role in the reabsorption of lung fluid. Improper fluid reabsorption at birth leads to a condition called respiratory distress syndrome which is the leading cause of death among newborns. Our procedure involved supporting the lungs in vitro for a duration of three hours in Krebs' saline and the rates of fluid production were measured using a dye-dilution technique. The control rates ranged from 0.98 to 1.34 ml/kg*hr with gestational ages between 59 to 65 days (gestation is 67 days) which is comparable to rates reported from fetal sheep. The lungs were exposed to different concentrations of epinephrine, ranging from 10⁻⁸ M to 10⁻⁵ M, during the second hour of experimentation, following an ABA design. Epinephrine produced reductions in fluid secretion in a dose dependent manner except at pharmacological levels where the response disappeared. Optimal responses to epinephrine were obtained at 10⁻⁷ M. The unexpected results at high concentrations of epinephrine warranted further investigation using specific alpha-adrenergic receptor blockers. However, tests with general alpha and beta-adrenergic receptor antagonists were carried out beforehand to confirm previous work which showed that epinephrine works through alpha and not beta receptors. Propranolol, a general beta blocker, did not block the effect of 10⁻⁷ M epinephrine whereas phentolamine, a general alpha blocker, eliminated the effect of epinephrine. Thus, epinephrine in the fetal guinea pig lung appears to work through alpha-adrenergic receptors rather than beta-adrenoreceptors. Experiments with specific alpha-adrenoreceptor antagonists have suggested that epinephrine stimulates two opposing mechanisms at high pharmacological concentrations while at physiological levels, epinephrine stimulates a single process. Studies with yohimbine (10⁻⁴ M), a specific alpha₂~adrenoreceptor antagonist, and epinephrine at 10⁻⁵ M as well as 10⁻⁷ M suggest that alpha₁-receptor stimulation causes a significant increase in lung fluid secretion. This is the first reported case where an increase in lung liquid production was obtained on a consistent basis. Tests with prazosin (10⁻⁵ M), a specific alphas-receptor blocker, and epinephrine (10-* M) appears to show that alpha₂-receptor stimulation cause a significant reduction in lung liquid secretion. However, the lack of an effect of prazosin (10⁻⁵ M) at physiological levels of epinephrine (10~7 M) implies that alpha₁-receptors function only at pharmacological levels. Therefore, at physiological levels of epinephrine, only alpha₂_adrenoreceptors are activated to reabsorb lung liquid and at pharmacological levels, two opposing mechanisms (alpha₁ and alpha₂-adrenoreceptors) are stimulated to eliminate the effects of epinephrine.

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