title: Chronic hypoxia alters vasoconstrictive responses of femoral artery in the fetal sheep.
abstract: The purpose of this study was to determine if mild hypoxia alters the responsiveness to vasoactive agents in the renal and the femoral arteries in the fetal sheep. Ten pregnant sheep were operated under halothane anesthesia at 116 to 124 days' gestation. A maternal tracheal catheter was placed for infusing compressed air (control group, n=5) or nitrogen (hypoxia group, n=5) starting on post operative day 6 and maintained for 5 days. Femoral and renal arteries were harvested from the fetus to study the constriction response to phenylephrine (PE 10(-9) to 10(-5)mol/L). To determine the involvement of nitric oxide as a modulator of vessel constriction, N-nitro-L-arginine methyl ester (L-NAME) was used at a concentration of 10 -4 mol/L in parallel chambers. In the hypoxia group, maternal PaO2 significantly decreased from a base-line of 110.4+/-1.4 to 80.5+/-1.6 (mmHg, p<0.01), fetal PaO2 significantly decreased from a baseline of 20.9+/-0.3 to 15.5+/-0.1 (mmHg, p<0.01). Hypoxia was associated with a significant increase in PE maximal response in the absence (184.5+/-6.6 vs. 146.2+/-4.3) and presence (166.9+/-6.3 vs. 145.0+/-4.5) of L-NAME, and a decrease in EC50 in the absence (6.0+/-1.1 vs. 27.0+/-4.1) of L-NAME of femoral arteries. However, there were no significant differences in PE maximal response and EC50 in the absence and presence of L-NAME of renal arteries. We concluded that mild chronic hypoxia seems to increase the fetal femoral artery response to PE, but not in the fetal renal artery. This observation is consistent with a redistribution of cardiac output away from the carcass.
authors.affiliation: Departments of Obstetrics and Gynecology, Chonnam National University Medical School, Gwangju, Korea. kimyh@chonnam.ac.kr
authors.forename: Yoon Ha
authors.initials: YH
authors.lastname: Kim
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Veille
authors.forename: Moon Kyoung
authors.initials: MK
authors.lastname: Cho
authors.forename: Myoung Seon
authors.initials: MS
authors.lastname: Kang
authors.forename: Cheol Hong
authors.initials: CH
authors.lastname: Kim
authors.forename: Tae-Bok
authors.initials: TB
authors.lastname: Song
authors.forename: Jorge P
authors.initials: JP
authors.lastname: Figueroa
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005263:Femoral Artery / Q000196:embryology* / Q000473:pathology*; D006400:Hematocrit; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia; D007668:Kidney / Q000098:blood supply; D007773:Lactates / Q000097:blood / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010656:Phenylephrine / Q000737:chemistry / Q000378:metabolism / Q000494:pharmacology; D012077:Renal Artery / Q000473:pathology; D012756:Sheep / Q000196:embryology*; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D001786:Blood Glucose; D004791:Enzyme Inhibitors; D007773:Lactates; D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester
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