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Adenosine mediates metabolic and cardiovascular responses to hypoxia in fetal sheep.
Author(s) -
Koos B J,
Chau A,
Ogunyemi D
Publication year - 1995
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1995.sp021007
Subject(s) - hypoxia (environmental) , fetus , medicine , adenosine , bradycardia , metabolic acidosis , endocrinology , adenosine receptor antagonist , acidosis , adenosine receptor , anesthesia , blood pressure , heart rate , biology , oxygen , chemistry , receptor , pregnancy , organic chemistry , genetics , agonist
1. In seven unanaesthetized fetal sheep (> 80% term), isocapnic hypoxia (arterial partial pressure of O2, Pa,O2, approximately 15 mmHg) was induced for 1 h by lowering maternal inspired PO2. Fetal hypoxia was also produced during intra‐arterial administration of the adenosine receptor antagonist 8‐(p‐sulphophenyl)‐theophylline (8‐SPT). The fetal 8‐SPT infusion was begun just prior to hypoxia and was stopped when fetal Pa,O2 was returned to normal. 2. Hypoxia induced a progressive fetal acidosis, a rise in mean arterial pressure, a transient fall in heart rate and a decrease in breathing movements. 8‐SPT significantly reduced the metabolic acidosis and abolished the hypertension and bradycardia without altering hypoxic inhibition of fetal breathing. Administration of the vehicle for 8‐SPT during hypoxia did not significantly affect the normal fetal metabolic and cardiovascular responses to acute O2 deprivation. 3. It is concluded that adenosine mediates the fetal bradycardia and hypertension produced by hypoxia, indicating that adenosine modulates fetal autonomic responses to acute oxygen deficiency. Secondly, adenosine contributes to fetal metabolic acidaemia, suggesting that adenosine also modulates fetal glycolytic responses to hypoxia.