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Am J Physiol 231: 426-429, 1976;
0002-9513/76 $5.00
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American Journal of Physiology, Vol 231, Issue 2, 426-429
Copyright © 1976 by American Physiological Society


ARTICLES

Degradation of prostaglandin E2 and F2alpha by the canine liver

FL Anderson, W Jubiz, and TJ Tsagaris

Degradation of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha) by the liver was determined in 16 dogs. PGE2 (8 dogs) or PGF2 alpha (8 dogs) was infused into the left ventricle at rates of 3.75, 7.5, 15, 37.5, and 75 mug/min. Blood samples obtained simultaneously from the portal vein (PV), hepatic vein (HV), and abdominal inferior vena cava (IVC) at each infusion rate were tested for PGE or PGF concentration by radioimmunoassy. During PGE2 infusion the mean PGE concentrations in the PV were 0.60, 1.05, 1.40, 2.29, 4.80, and 7.29 ng/ml at each infusion rate, Corresponding concentrations in the HV were 0.51, 0.62, 0.71, 0.96, 1.94, and 2.62 ng/ml, and in the IVC 0.51, 0.95, 1.31, 1.96, 4.31, AND 5;18 NG/ML. During PGF2 alpha infusion, the mean PGF concentrations in the PV were 0.32, 0.59, 0.73, 1.73, 4.11, and 7.11 ng/ml at the respective infusion rates; Corresponding concentrations in the HV were 0.26, 0.24, 0.33, 0.48, 0.49, and 0.96 ng/ml, and in the IVC 0.32, 0.50, 0.61, 1.10, 2.40, and 4.17 ng/ml. Thus, these data indicate that the canine liver has substantial, but not unlimited, capacity for degradation of PGE2 and PGF2 alpha in the portal circulation. Whether or not PGE or PGF levels in the PV may exceed this capacity during periods of stress or whether this enzymatic mechanism may be suppressed by either physiological or pharmacological factors is not known.





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