TY - JOUR
T1 - Failure of acute hypoxia to alter pulmonary prostaglandin metabolism in dogs
AU - Moon, Mary A.
AU - Lemen, Richard J.
AU - Quan, Stuart F.
N1 - Funding Information:
ACKNOWLEDGMENTS These studies were supported by Nat3.onal Heart, Lung, and Blood Institute Grant HL23773 and a research grant from the Arizona Lung Association. M. A. Moon is a predoctoral student in physiology and was supported by National Institutes of Health Training Grant HLO7245. The authors would like to thank Melissa Whitten for her assistance in doing the experiments, and Marlene Smith for her secretarial expertise.
PY - 1983/5
Y1 - 1983/5
N2 - We studied the effects of acute hypoxia (Fi02=0.09-0.11, 20 min,.) on transpulmonary plasma prostaglandin (PG) concentrations in ten anaesthetized, paralyzed, artificially ventilated dogs. Concentrations of 6-keto-PGF1α, TxB2, PGE2, PGF2α, and 13, 13-dihydro-15-keto-PGF2α were measured from the pulmonary artery and abdominal aorta using radioimmunoassay. In an additional six dogs, the effects of arachidonic acid (AA) infusions (100 mg/kg/min) during normoxia and acute hypoxia were determined. Compared to normoxic conditions, acute hypoxia increased pulmonary artery pressure (p<0.0), decreased both the arterial oxygen tension (Pa02) and the alveolar-to-arterial oxygen tension gradient (A-aD02) (p <0.05), but did not affect transpulmonary plasma PG concentrations. AA infusions significantly (p <0.05) increased 6-keto-PGF1α independent of Fi02. Acute hypoxia failed to elicit a pulmonary pressor response in the AA-treated animals although Pa02 and A-aD02 decreased (p<0.5). These data in healthy dogs suggest that (1) acute hypoxia does not alter net pulmonary PG metabolism, (2) prostacyclin synthesis is stimulated by increased plasma AA concentrations and (3) this effect may block normal pressor responses to hypoxic stimuli.
AB - We studied the effects of acute hypoxia (Fi02=0.09-0.11, 20 min,.) on transpulmonary plasma prostaglandin (PG) concentrations in ten anaesthetized, paralyzed, artificially ventilated dogs. Concentrations of 6-keto-PGF1α, TxB2, PGE2, PGF2α, and 13, 13-dihydro-15-keto-PGF2α were measured from the pulmonary artery and abdominal aorta using radioimmunoassay. In an additional six dogs, the effects of arachidonic acid (AA) infusions (100 mg/kg/min) during normoxia and acute hypoxia were determined. Compared to normoxic conditions, acute hypoxia increased pulmonary artery pressure (p<0.0), decreased both the arterial oxygen tension (Pa02) and the alveolar-to-arterial oxygen tension gradient (A-aD02) (p <0.05), but did not affect transpulmonary plasma PG concentrations. AA infusions significantly (p <0.05) increased 6-keto-PGF1α independent of Fi02. Acute hypoxia failed to elicit a pulmonary pressor response in the AA-treated animals although Pa02 and A-aD02 decreased (p<0.5). These data in healthy dogs suggest that (1) acute hypoxia does not alter net pulmonary PG metabolism, (2) prostacyclin synthesis is stimulated by increased plasma AA concentrations and (3) this effect may block normal pressor responses to hypoxic stimuli.
UR - http://www.scopus.com/inward/record.url?scp=0020623647&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0020623647&partnerID=8YFLogxK
U2 - 10.1016/0090-6980(83)90116-8
DO - 10.1016/0090-6980(83)90116-8
M3 - Article
C2 - 6577520
AN - SCOPUS:0020623647
SN - 0090-6980
VL - 25
SP - 615
EP - 627
JO - Prostaglandins
JF - Prostaglandins
IS - 5
ER -