Alveolar fluid clearance in late-gestational guinea pigs after labor induction: mechanisms and regulation
absorption; adrenaline; alveolar epithelium; beta-adrenergic stimulation; birth; catecholamines; developmental-changes; distress syndrome; epinephrine; fetal sheep; infant respiratory; lung liquid clearance; newborn rabbits; Physiology; prenatal development; Respiratory System; sodium transport; transport; ventilated rats
We tested the hypothesis that labor-induced epinephrine release would stimulate alveolar fluid clearance in preterm fetuses. Preterm fetuses were obtained by cesarean section from timed-pregnant guinea pigs at 61-69 days postconception. Fetal guinea pigs were euthanized and placed on continuous positive airway pressure oxygenation, and an isosmolar 5% albumin solution was instilled. Alveolar fluid clearance was measured over 1 h. The fetal lung began to absorb fluid at 64-66 days postconception, and at birth, alveolar fluid clearance quadrupled. Baseline alveolar fluid clearance when present was sensitive to propranolol inhibition and depended on beta -adrenergic stimulation. Measurements of plasma epinephrine in fetal animals confirmed high epinephrine levels in 66- to 69-day postconception fetuses. Prenatal alveolar fluid clearance when present was highly amiloride sensitive, suggesting that amiloride-sensitive Na+ channels were critical. Oxytocin-induced labor initiated an amiloride- and propranolol-sensitive net alveolar fluid clearance in 61-day-gestation animals. Moreover, oxytocin induced significant epinephrine release in all fetuses. These results have clinical implications for infants delivered by cesarean section before the onset of labor. Use of pharmacological agents to induce labor may reduce the occurrence and severity of perinatal respiratory distress.
Norlin A; Folkesson H G
American Journal of Physiology-Lung Cellular and Molecular Physiology
2001
2001-04
Journal Article
<a href="http://doi.org/10.1152/ajplung.2001.280.4.l606" target="_blank" rel="noreferrer noopener">10.1152/ajplung.2001.280.4.l606</a>
HORMONAL-CONTROL OF GROWTH IN THE GENETICALLY-OBESE ZUCKER RAT .1. LINEAR GROWTH, PLASMA INSULIN-LIKE GROWTH FACTOR-I (IGP-I) AND IGF-BINDING PROTEINS
body-composition; developmental-changes; Endocrinology & Metabolism; expression; gh; hepatocytes; messenger-rna; radioimmunoassay; secretion; serum; somatomedin-c
The genetically obese Zucker rat is a widely used model of early-onset obesity. Like obese children, these obese rats are hyperinsulinemic and have low GH secretion. However, data on linear growth and insulin-like growth factor-I (IGF-I) levels in this model are scanty and contradictory. In the present study, we investigated linear growth and its hormonal control in Zucker rats (male and female) from 4-20 weeks of age. In the obese animals, compared to their lean littermates, the naso-anal length was normal or slightly greater, whereas the tails and femurs were shorter. The plasma concentration of IGF-I increased between 4-20 weeks of age, and IGF-I levels were normal or slightly higher in the obese animals. The serum level of IGF-binding protein-3 (IGFBP-3) measured by Western ligand blotting was not significantly different in lean vs, obese rats. To assess the IGF-I response to GH, bovine GH was administered (250 mu g/100 g BW, ip, daily for 3 days) to 16- to 20-week-old female Zucker rats; plasma IGF-I concentrations increased more in the obese (percent increase over baseline, 347 +/- 44% vs. 194 +/- 31%; P < 0.01). These results show that despite low GH secretion, genetically obese Zucker rats have 1) normal linear (nasoanal) growth, 2) normal or increased circulating levels of IGF-I and IGFBP-3, and 3) increased plasma IGF-I responses to exogenous GH. These results suggest that the GH-independent growth in this model could result from direct effects of hyperinsulinism on circulating IGF-I and IGFBP-3 levels and/or indirect effects through increased GH receptor function.
Nguyenyamamoto L; Deal C L; Finkelstein J A; Vanvliet G
Endocrinology
1994
1994-03
Journal Article
<a href="http://doi.org/10.1210/en.134.3.1382" target="_blank" rel="noreferrer noopener">10.1210/en.134.3.1382</a>