Heparin metabolism and heparin-release lipase activity during long-term estrogen-progestin treatment.
Short-term oral contraceptive therapy has been reported to decrease postheparin lipolytic activity (PHLA). Resistance to heparin has been held responsible for this effect. To test several alternative explanations, we studied both PHLA and heparin concentrations in nine control women and nine women receiving long-term estrogen-progestin therapy after they were given heparin intravenously (10 units/kg). There were no significant differences in the concentration of heparin, its rate of disappearance, or calculated space of distribution between control and treated groups. PHLA was depressed (p less than 0.05) by approximately 50% during long-term estrongen-progestin therapy. PHLA disappearance was similar in both groups. Thus, reduced PHLA in women receiving long-term oral contraceptive therapy cannot be related to altered heparin metabolism or to accelerated enzyme disappearance from plasma. Long-term estrogen-progestin administration may decrease the heparin-facilitated release of individual triglyceride hydrolase activities or enhance the affinity of enzyme binding to tissues.
D003276:Contraceptives, Oral / Q000494:pharmacology*; D003864:Depression, Chemical; D045166:Estradiol Congeners / Q000494:pharmacology*; D004997:Ethinyl Estradiol / Q000494:pharmacology; D005260:Female; D006493:Heparin / Q000378:metabolism*; D006801:Humans; D008049:Lipase / Q000378:metabolism*; D008656:Mestranol / Q000494:pharmacology; D009640:Norethindrone / Q000494:pharmacology; D009641:Norethynodrel / Q000494:pharmacology; D009644:Norgestrel / Q000494:pharmacology; D045167:Progesterone Congeners / Q000494:pharmacology*; D013997:Time Factors; D014280:Triglycerides / Q000378:metabolism
D003276:Contraceptives, Oral; D045166:Estradiol Congeners; D045167:Progesterone Congeners; D014280:Triglycerides; D009644:Norgestrel; D004997:Ethinyl Estradiol; D009641:Norethynodrel; D006493:Heparin; D008656:Mestranol; D008049:Lipase; D009640:Norethindrone