Background: Fecondation invitro is an outstanding scientific progression in the 20th century. Beside the technical factor and choosing a schedule to reach the fertility rate of high pregnancy, the thickness of uterine endothelium can\u2019t be let pass unnoticed because it is a favorable factor for the embryons which can made easily the foyer in the uterine. Objective: To define the relation between the thickness of uterine endothelium with a concentration of estradiol plasma in the day when injecting hCG with the result of pregnancy. Subject and Method: A retrospective study with research in to 294 cases of IVF. Result: 58.9% is secondary infertile with the average age between 32.6 +/-5.4 who have been infertile in the timescale of 6.4+/-5.0 years. Injecting hCG to take ovocyte when the average estradiol concentradiol is 2378 +/- 1335.9 pg/ml and the estradiol concentration of ovule is 251.4pg/ml. Conclusion: The higher the estradiol concentration is, the thicker the uterine endothelium is. 7.3% cases had uterine endothelium thicker than 10mm if the estradiol concentration is higher than 3000pg/ml. The rate of people who are clinically pregnant with the uterine endothelium > 10mm is 2.24 times higher than the rate of people who are clinically pregnant with the uterine endothelium < 10mm.
Infertile ; Fecondation invitro (IVF) ; Uterine endothelium ; Clinically pregnant.

OBJECTIVES: The present study was performed to investigate whether estrogen and progesterone induce the change of vascular tone in endothelium-denuded human uterine artery and vascular reactivity may be mediated by intracelluar calcium modulation through receptor- and voltage-dependent calcium channels. METHODS: The uterine arteries were obtained at the time of hysterectomy from 28 women followed by denudation of endothelium. After confirmation of functional integrity of endothelium-denuded uterine artery, vascular reactivity was measured by using isometric force transducer and recorded by physiograph. Contraction was induced by 10-6 M norepinephrine and 35mM high concentrated potassium chloride solution which activated receptor-dependent calcium channel and voltage-dependent calcium channel, respectively.Thereafter estradiol of 4 different concentrations from 3x10-11M to 3x10-8M was administered. Progesterone was also administered to endothelium-denuded uterine artery which was contracted by 10-6M norepinephrine and high potassium chloride solution. To evaluate the effect of additional progesterone on vascular smooth muscle relaxation effect of estrogen,4 different progesterones in concentrations from 3x10-8M to 3x10-5M were given to vascular smooth muscle which was initially pretreated with norepinephrine followed by relaxation of estradiol. RESULTS: Estradiols from 3x10-11M to 3x10-8M showed in significant dose-dependent vascular relaxation. Progesterones result in significant decrease in vascular contraction in concentration dependent manner. Additional progesterone on estrogenic effects also results in significant decrease in vascular contraction. CONCLUSION: Estradiol may have endothelium independent vasorelaxation effect in human uterine artery. These vasorelaxant effects may be mediated through antagonistic action for receptor-and voltage-dependent calcium channels in vascular smooth muscle. Progesterone also bring about vasorelaxation by same action in endothelium-denuded vascular smooth muscle. On estrogen induced vascular relaxation, progesterone results in additional vasorelaxation.
Calcium ; Calcium Channels ; Endothelium ; Estradiol ; Estrogens* ; Female ; Humans* ; Hysterectomy ; Muscle, Smooth, Vascular ; Norepinephrine ; Potassium Chloride ; Progesterone* ; Relaxation ; Transducers ; Uterine Artery* ; Vasodilation

OBJECTIVE: This study was performed to investigate whether 1) progestogens induce changes of vascular tone in endothelium-denuded smooth muscles of human uterine artery, 2) endothelium-independent vascular reactivity is mediated by intracelluar calcium ion modulation through 2 types of calcium channel, both voltage- and receptor-dependent and 3) 3 kinds of progestogen such as a progesterone, C19 nortestosterone(norethindrone acetate ; NETA) and C21 progestogen(medroxyprogesterone acetate ; MPA), have a different vasoreactivity. METHODS: The uterine arteries were obtained at the time of hysterectomy from 24 women who had no cardiovascular disease risk factors and the endothelium was denuded. Vascular reactivity was monitored by using isometric force transducer and recorded by physiograph. Endothelial integrity was assessed by adding 10micrometer acetylcholine(endothelium-dependent vasorelaxant) to the specimens, which were pretreated with 1micrometer norepinephrine(alpha-adrenergic stimulant). The integrity of smooth muscle was assessed by adding 10micrometer sodium nitroprusside(endotelium -independent vasorelaxant) and 10micrometer tamsulosin(alpha-adrenergic blocker) to the specimens, pretreated with 1micrometer norepinephrine. The uterine smooth muscles were pretreated with 35mM and 70mM potassium chloride and 10-7M and 10-6M norepinephrine. Three kinds of progestogen - progesterone, NETA and MPA - each at 5 different concentrations(10-9g/ml, 10-8g/ml, 10-7g/ml, 10-6g/ml and 10-5g/ml) were used. RESULTS: The loss of endothelial function and adequacy of smooth muscle function were confirmed. Three kinds of progestogen had concentration-dependent inhibitory effects on vascular smooth muscle contr action induced by high potassium solution and norepinephrine, respcetively. There were no siginificant differences noted among the inhibitory effects of three progestogens in 35mM concentration of potassium solution and 10-6M norepinephrine induced muscular contraction. In 70mM potassium solution, there were significant differences among the three progestogens-induced inhibitory effects. Progesterone showed the most potent inhibitory effect, NETA was intermediate, and MPA had the mildest effect. In 10-7M norepinephrine, progesterone had more potent inhibitory effect than NETA or MPA. The difference between progesterone and NETA/MPA was statistically siginificant, with no significance between NETA and MPA. CONCLUSION: The results of this study revealed that progestogens have a concentration-dependent vaso-relaxant effect on endothelium-denuded vasular smooth muscles via a calcium antagonistic mechanism of direct inhibitory effects on receptor- and voltage-dependent calcium ion channels. This vaso-relaxant effect of progestogens differed among a variety of progestogens. In conclusion, the progestogens combined with estrogens have not antagonistic effect on vaso-relaxation at least and maybe have synergistic effect with estrogens, in vivo.
Calcium ; Calcium Channels ; Cardiovascular Diseases ; Endothelium ; Estrogens ; Female ; Humans* ; Hysterectomy ; Muscle Contraction ; Muscle, Smooth ; Muscle, Smooth, Vascular* ; Norepinephrine ; Potassium ; Potassium Chloride ; Progesterone ; Progestins* ; Risk Factors ; Sodium ; Transducers ; Uterine Artery

OBJECTIVE: This study was performed to investigate whether 1) estrogen induces the change of vascular tone in endothelium-denuded human uterine artery, and 2) endothelium-independent vascular reactivity may be mediated by intracellular calcium ion modulation. METHODS: The uterine arteries from 34 premenopausal women were obtained at the time of hysterectomy due to various indications and endothelium was denuded. Vascular reactivity was monitored by using Isometric force transducer and recorded by physiograph. Endothelial integrity was assessed by sequential administration of 1micrometer norepinephrine(alpha-adrenergic stimulant) and 10 micrometer acetylcholine (endothelium -dependent vasorelaxant). Integrity of smooth muscle was measured by administration of 10 micrometer sodium nitroprusside (endothelium - independent vasorelaxant) and 10 micrometer tamsulosin(alpha-adrenergic blocker). A dose-dependent action of estrogen was measured on denuded uterine arteries, pretreated with norepinephrine and potassium chloride. In media contained denuded uterine arteries pretreated with 70mM potassium chloride and estradiol(3X10-5M), nitric oxide and its inhibitor, N-nitro-L-arginine methyl ester(L-NAME) was administered, respectively, in order to verify the vasodilation effect. Statistical tests were performed at the 5% level of significance using the SPSS PC+ package. RESULTS: Acethylcholine has little effect but sodium nitroprusside & talmsulosin showed marked relaxation, which suggested loss of endothelial function and adequacy of smooth muscle function. The contraction by norephinephrine(1 M) revealed estrogen induced relaxation which was concentration-dependent from 3 10-8M to 3 10-5M in concentration of 17 -estradiol. The contraction by high potassium solution 70mM was also inhibited by estrogen in concentration-dependent manner. This vasorelaxant effect of estrogen on endothelium-denuded uterine artery was not affected by addition of nitric oxide(NO) precursor, L-arginine and nitric oxide synthase(NOS) inhibitor, L-NAME. CONCLUSION: The results of this study revealed that estrogen has vasorelaxant effect on endothelium endothelium-denuded uterine artery by calcium antagonistic property through direct inhibitory effect on receptor- and voltage dependent calcium ion channels of smooth muscles. This vasorelaxant effect of estrogen on endothelium-denuded uterine artery was NO independent.
Acetylcholine ; Arginine ; Calcium ; Calcium Channels ; Endothelium* ; Estrogens* ; Female ; Humans* ; Hysterectomy ; Muscle, Smooth ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Nitroprusside ; Norepinephrine ; Potassium ; Potassium Chloride ; Relaxation ; Transducers ; Uterine Artery* ; Vasoconstriction* ; Vasodilation

Adolescent ; Adult ; Breast Neoplasms ; pathology ; Carcinoma ; pathology ; Diagnosis, Differential ; Endothelium, Vascular ; pathology ; Fasciitis ; pathology ; Female ; Hemangiosarcoma ; pathology ; Histiocytoma, Malignant Fibrous ; pathology ; Humans ; Hyperplasia ; pathology ; Leiomyoma ; pathology ; Leiomyosarcoma ; pathology ; Middle Aged ; Soft Tissue Neoplasms ; pathology ; Uterine Neoplasms ; pathology ; Vascular Diseases ; pathology