The effect of fertility stress on endometrial and subendometrial blood flow among infertile women

Abstract

BackgroundTo investigate the effect of fertility stress on endometrial and subendometrial blood flow among infertile women.MethodsThis case–control study was conducted in The First Affiliated Hospital of Zhengzhou University. The fertility problem inventory (FPI) was adopted to evaluate fertility stress. Three-dimensional power Doppler ultrasonography (3D PD-US) was performed during the proliferative phase of the menstrual cycle (days 5–11) to measure endometrial thickness, pattern, endometrial and subendometrial volume (V), the vascularization index (VI), the flow index (FI) and the vascularization-FI (VFI) index. Then, 300 infertile women were separated into two groups (high-score group and low-score group) based on total FPI scores and 80 healthy women were selected as controls.ResultsNo differences were found among all three groups with regard to general characteristics, endometrial thickness, pattern, endometrial and subendometrial V, VI and VFI. The endometrial and subendometrial FIs associated with different stress levels significantly differed among the three groups (F = 33.95, P < 0.001; F = 44.79, P < 0.001, respectively). The endometrial and subendometrial FIs in the control group were significantly higher than those in the high-score group and low-score groups. The endometrial and subendometrial FIs in the low-score group were significantly higher than those in the high-score group. The total FPI score was closely related to the endometrial and subendometrial FIs (r = −0.304, P < 0.001; r = −0.407, P < 0.001, respectively).ConclusionFertility stress was associated with endometrial and subendometrial flow index. Whether fertility stress might affect pregnancy outcome by reducing endometrial and subendometrial blood flow requires further research.

IVF and other ART in low- and middle-income countries: a systematic landscape analysis

“…In addition, national and regional registries are attempting to collect data on ART treatments, with some success in Latin America and Africa ( Zegers-Hochschild et al , 2013 ; SARA report, 2014 ; Zegers-Hochschild et al , 2014 ; et al , 2015; et al , 2016). More rigorous data reporting, collection and verification are needed from LMIC to enable a meta-analysis in the future ( Kushnir et al , 2017 ).…”

Differential role of r-met-hu G-CSF on male reproductive function and development in prepubertal domestic mammals

“…Experimental efforts have previously hinted the in vivo role of G-CSF on spermatogenesis. Accordingly, GC depleting effects by cytotoxic drugs [19,20] or radiation [38] were reversed with G-CSF. We tested r-met-hu G-CSF during pre-puberty, a time window on which GCs expand and differentiate in a divergent way with intense germ stem cell activity.…”

“…Moreover, G-CSF receptor CSF3R has been identified in murine SSCs [19]. Testicular damage from chemotherapy influence the physiological regeneration of male GCs in the testis [20,21], up to a limit imposed by Sertoli cell numbers [20] and G-CSF seems to have a protective role in radiation-induced testicular impairment [21] Currently, there are several types of human recombinant G-CSF (rhG-CSF) commercially available for clinical applications [22–24]. The non-glycosylated r-met-hu G-CSF, known as r-met-hu/G-CSF, has been successfully used to stimulate proliferation and maturation of hematopoietic cells [11,25].…”

Fertility Massage: an Unethical Practice?

“…( 6 ) Stress can also affect the hypothalamic-pituitary-ovarian axis by reducing hypothalamic gonadotropin-releasing hormone secretion, in turn reducing pituitary secretion of luteinizing hormone and follicle-stimulating hormone, thereby reducing ovarian hormone synthesis and, in some cases, ovulation. ( 7 ) Psychological stress increases the concentration of glucocorticoids and catecholamines ( 8 ) which can excite catecholamines alpha receptors and cause vasoconstriction, thereby reducing uterus blood flow ( 7 ) which may reduce endometrial and sub-endometrial blood flow and thus pregnancy outcomes (both in IVF and non-IVF pregnancy attempts). ( 7 ) In addition, research has shown that psychological stress can trigger embryonic death.…”

“…( 7 ) Psychological stress increases the concentration of glucocorticoids and catecholamines ( 8 ) which can excite catecholamines alpha receptors and cause vasoconstriction, thereby reducing uterus blood flow ( 7 ) which may reduce endometrial and sub-endometrial blood flow and thus pregnancy outcomes (both in IVF and non-IVF pregnancy attempts). ( 7 ) In addition, research has shown that psychological stress can trigger embryonic death. ( 9 – 11 ) The exact mechanism for this loss is unknown, but a decrease in pregnancy-protective cytokines, a reduction in progesterone and prolactin, and elevated glucocorticoids are all thought to contribute to stress-triggered pregnancy loss such as miscarriage.…”