Mechanism whereby nitric oxide (NO) infused chronically intrauterine in ewes is antiluteolytic rather than being luteolytic.

摘要: Nitric oxide (NO) has been reported to be luteolytic in vitro and vivo cows. However, an NO donor reversed PGF2alpha-induced inhibition of rat luteal progesterone secretion or endothelin-1 stimulated bovine tissue prostaglandins E (PGE; PGE1, PGE2) without affecting PGF2alpha secretion. In addition, chronic infusion into the interstitial ovarian vascular pedicle adjacent luteal-containing ovary prevented decline circulating progesterone, while a nitric synthase (NOS) inhibitor did not affect luteolysis. The objective this experiment was determine whether NOS infused chronically intrauterine during ovine estrous cycle antiluteolytic. Ewes were treated either with vehicle (N=5), diethylenetriamine (DETA-control for DETANONOate; N=5), (Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETANONOate-long acting donor; N=6), l-arginine l-nitro-arginine methyl ester (l-NAME-NOS inhibitor; NG-monomethyl-l-arginine acetate (l-NMMA; N=5) every 6h from 2400h (0h) on day 8 through 1800h 18 cycle. Jugular venous blood inferior vena cava plasma via saphenous vein cathether 5cm anterior juncture collected analysis PGE, respectively, by RIA. Corpora lutea at weighed. Weights corpora heavier (P =0.05). Profiles jugular days 8-18 differed =0.05) amongst each other. PGE:PGF2alpha ratio profile DETANONOate-treated ewes increased (P< when compared all other treatment groups. second experiment, conversion [3H PGE2] PGF2alpha] 15 caruncular endometrium determined vehicle, DETA, DETANONOate-treatment Conversion decreased only DETANONOate. It is concluded that cycle, but may instead antiluteolytic prevent luteolysis altering secreted uterus.